最新刊期

    32 15 2026
    • WANG Ting, GUO Zhaojuan, DU Shouying, TU Can, ZHANG Lin
      Vol. 32, Issue 15, Pages: 1-13(2026) DOI: 10.13422/j.cnki.syfjx.20261328
      摘要:Ancient classical formulas, the essence of traditional Chinese medicine (TCM) theory and clinical practice, serve as a vital vehicle for TCM inheritance and innovation. Following the recent reform of TCM review and approval system, the number of approved TCM compound prescriptions derived from ancient classical formulas has been steadily increasing. Based on a review of the developmental trajectory of these prescriptions, this paper summarizes the current status of research and development in this field, including a limited scope of clinical application, a "clustering" of research and registration applications for certain varieties, risks exposed in non-clinical safety studies of individual varieties, and the absence of approved ethnic medicine-derived ancient classical formulas for marketing. Then, an in-depth analysis is conducted on issues requiring attention during the research and development process, including the difficulty in key information verification, multiple origins and the lack of quality standards for some medicinal materials, the inclusion of potentially toxic Chinese medicinal materials in formulations, as well as rare applications in modern clinical practice and quality control challenges for certain dosage forms. In light of the current status of research, development, and regulation, the following recommendations are proposed: ① Strengthen key information verification by integrating compliance with ancient literature records and contemporary regulatory requirements; ②Enhance the research and formulation of medicinal material standards to ensure uniformity, stability, and quality controllability of marketed Chinese patent medicines; ③ Intensify dosage form process research and quality standard evaluation to guarantee preparation safety and efficacy while adhering to ancient prescriptions; ④ Pay attention to potentially toxic Chinese medicinal materials, animal models for toxicity evaluation, and interspecies toxicity differences in animals, and carefully select animal species for non-clinical safety evaluations, with additional species included when necessary; ⑤ Actively analyze the pharmacodynamic substance basis and mechanisms of ancient classical formulas to "clearly elucidate" their scientific connotation; ⑥ Strengthen post-marketing clinical research, refine clinical positioning, and continuously improve the effectiveness and safety information included in package inserts. Based on the current status of research and development of ancient classical formulas, this paper aims to analyze the issues requiring attention during their research and development and to propose scientific regulatory recommendations, so as to provide references for promoting the research, development, and scientific supervision of relevant prescriptions.  
      关键词:ancient classical formula;traditional Chinese medicine (TCM) compound prescription;research and development of new TCM drug;scientific regulation of TCM;"three-combination" review evidence system   
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    • LIU Yu, ZHANG Meiling, SONG Nan, ZHU Jingxuan, SUN Xiaofei, JU Xing, MIN Dongyu
      Vol. 32, Issue 15, Pages: 14-25(2026) DOI: 10.13422/j.cnki.syfjx.20251511
      摘要:ObjectiveThis paper aims to construct a ceRNA regulatory network related to microRNA-342-3p (miR-342-3p) and to investigate the molecular mechanism by which Danlou tablets (DLT) ameliorate hepatic lipid deposition by regulating circular RNA cysteine-rich transmembrane BMP regulator 1 (circCRIM1)/miR-342-3p/SRY-box transcription factor 6 (SOX6)-mediated fatty acid synthesis.MethodsA ceRNA regulatory network related to miR-342-3p was constructed using databases. The targeting relationships between circCRIM1/miR-342-3p and miR-342-3p/SOX6 were verified using a dual-luciferase reporter assay. In vivo, C57BL/6 mice served as the blank control group and were fed a normal diet. Apolipoprotein E-deficient (ApoE-/-) mice were randomly divided into a model group, low-, medium-, and high-dose DLT (DLT-L, DLT-M, DLT-H) groups (340, 680, 1 360 mg·kg-1·d-1, respectively), and a simvastatin group (2.275 mg·kg-1·d-1). The ApoE-/- mice were fed a high-fat diet for 12 weeks to establish the model, with corresponding intragastric administration during the final four weeks. Serum lipid and liver function levels were measured using a fully automatic biochemical analyzer, and hepatic lipid levels were determined using kits. Histopathological changes in the liver tissue were observed using hematoxylin-eosin (HE) and oil red O staining. The expressions of circCRIM1 and miR-342-3p in liver tissue were detected by real-time polymerase chain reaction (Real-time PCR). The mRNA and protein expressions of SOX6, peroxisome proliferator-activated receptor γ (PPARγ), liver X receptor α (LXRα), and sterol regulatory element-binding protein 1c (SREBP1c) in the liver tissue of mice were measured by Real-time PCR and the Wes automated Western blot system, respectively. SOX6 protein expression in the liver tissue of mice was also assessed by immunohistochemistry. In vitro, a lipid deposition model was established by inducing HepG2 cells with oleic acid (OA). The cells were divided into a control (CON) group, an OA model group (400 μmol·L-1 OA), a blank serum (BS) group (400 μmol·L-1 OA + 10% BS), and a DLT group (400 μmol·L-1 OA + 10% DLT-containing serum). The lipid levels in HepG2 cells were measured using biochemical kits, and cellular morphological changes were observed with oil red O staining. The overexpression of circCRIM1 (OE-circCRIM1), miR-342-3p inhibition (miR-342-3p inhibitor), and DLT-containing serum were used to make the intervention. The expression levels of circCRIM1, miR-342-3p, and their corresponding mRNAs were measured by real-time PCR.ResultsIn vivo, compared with those in the CON group, the mice in the model group exhibited significantly abnormal serum lipids, liver function, and hepatic lipid levels (P<0.01), along with altered liver tissue structure, increased vacuoles, and increased lipid droplet accumulation. The expression of circCRIM1 was significantly upregulated, while that of miR-342-3p was significantly downregulated. The mRNA and protein expressions of SOX6, PPARγ, LXRα, and SREBP1c were all significantly increased (P<0.01). Compared with those in the model group, mice in all DLT groups with different doses showed significant improvements in serum lipids, liver function, and hepatic lipid levels (P<0.05, P<0.01), with attenuated liver damage and lipid droplet accumulation. The expression of circCRIM1 was decreased, and the expression of miR-342-3p was significantly increased. The mRNA and protein expressions of SOX6, PPARγ, LXRα, and SREBP1c were significantly reduced (P<0.05, P<0.01). In vitro, compared with the CON group, the OA group showed significantly increased lipid levels in HepG2 cells (P<0.01), with a greater number and larger size of lipid droplets. Treatment with DLT-containing serum ameliorated the changes. Overexpression of circCRIM1 significantly upregulated circCRIM1 and SOX6 mRNA, while downregulating miR-342-3p (P<0.05, P<0.01). Inhibition of miR-342-3p significantly elevated SOX6 mRNA and reduced miR-342-3p (P<0.01). DLT-containing serum markedly increased miR-342-3p and decreased SOX6, PPARγ, LXRα, and SREBP1c mRNA levels (P<0.01).ConclusionDLT can ameliorate hepatic lipid deposition and thereby prevent and treat atherosclerosis by regulating fatty acid synthesis via the circCRIM1/miR-342-3p/SOX6.  
      关键词:Danlou tablets;atherosclerosis;regulating circular RNA cysteine-rich transmembrane BMP regulator 1 (circCRIM1)/microRNA-342-3p (miR-342-3p) /SRY-box transcription factor 6 (SOX6);fatty acid synthesis;hepatic lipid deposition   
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    • LIU Yu, ZHANG Meiling, SONG Nan, LENG Yujie, SUN Xiaofei, ZHU Jingxuan, JIA Lianqun, MIN Dongyu
      Vol. 32, Issue 15, Pages: 26-34(2026) DOI: 10.13422/j.cnki.syfjx.20251514
      摘要:ObjectiveTo investigate the effects and molecular mechanisms of Danlou tablet (DLT) on hepatic lipid deposition in atherosclerotic (AS) mice, with a focus on autophagy mediated by the Sirtuin 6 (SIRT6)/cAMP response element-binding protein (CREB)/Neuron-derived orphan receptor 1 (Nor1) signaling pathway.MethodsEight C57BL/6 mice served as the control group. Forty-five Apolipoprotein E-deficient (ApoE-/-) mice were randomly divided into five groups: a model group, low-, medium-, and high-dose DLT groups (DLT-L, DLT-M, DLT-H; 340, 680, 1 360 mg·kg-1·d-1, respectively), and a simvastatin group (2.275 mg·kg-1·d-1). The AS model was established by administering a high-fat diet for 12 weeks. Concurrent with model establishment, the mice received their respective treatments via gavage for 4 weeks. Serum levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were measured using an automated biochemical analyzer. The concentrations of TG and non-esterified fatty acids (NEFA) in liver tissue were measured using microplate-based colorimetric methods. Histopathological changes in the liver were evaluated using hematoxylin-eosin (HE) and Oil Red O staining. Hepatic expression of SIRT6 was analyzed by immunohistochemistry. Real-time quantitative PCR (Real-time PCR) and a Wes Simple Western system were used to detect the mRNA and protein expression levels of SIRT6, Nor1, and key autophagy-related molecules, including Beclin1, autophagy-related protein 5 (ATG5), and UNC-51-like kinase 1 (ULK1).ResultsCompared with the control group, the model group exhibited significantly elevated serum levels of TC, TG, LDL-C, AST, and ALT, as well as increased hepatic TG and NEFA content, whereas serum HDL-C levels were significantly reduced (P<0.01). Histological examination revealed disordered hepatocyte arrangement, macrovesicular steatosis, and diffuse orange-red lipid droplets. The protein expression of phosphorylated CREB (p-CREB), CREB, and microtubule-associated protein 1 light chain 3 r (LC3 ge was decreased (P<0.01), and the mRNA and protein expressions of SIRT6, Nor1, Beclin1, ATG5, and ULK1 were also significantly downregulated in the model group (P<0.01). After intervention with DLT and simvastatin, the disordered hepatocyte arrangement and lipid deposition were ameliorated to varying degrees. Serum TC, TG, LDL-C, AST, and ALT levels, along with hepatic TG and NEFA content, were significantly decreased, while serum HDL-C levels were increased (P<0.05, P<0.01). Concurrently, the protein levels of p-CREB, CREB, and LC3 Ⅱ, as well as the mRNA and protein levels of SIRT6, Nor1, Beclin1, ATG5, and ULK1, were significantly upregulated (P<0.05, P<0.01). The therapeutic effects of DLT were dose-dependent, with the high-dose group demonstrating the most pronounced efficacy.ConclusionDLT can ameliorate hepatic lipid deposition and consequently prevent and treat AS by activating autophagy through the regulation of the SIRT6/CREB/Nor1 signaling pathway.  
      关键词:atherosclerosis;hepatic lipid deposition;Danlou tablet;Sirtuin 6 (SIRT6)/cAMP response element-binding protein (CREB)/Neuron-derived orphan receptor 1 (Nor1) signaling pathway;autophagy   
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    • SUN Xiaofei, SONG Nan, CAO Yuan, LIU Yu, ZHANG Meiling, ZHU Jingxuan, WANG Jiaxin, DONG Yuanguang, JIA Lianqun
      Vol. 32, Issue 15, Pages: 35-44(2026) DOI: 10.13422/j.cnki.syfjx.20251613
      摘要:ObjectiveThis paper aims to investigate the impact and underlying molecular mechanism of gypenosides (GPs) on improving lipid deposition in the liver of metabolic-associated fatty liver disease (MAFLD) mice.MethodsBy using databases including the Comparative Toxicogenomics Database, SwissTargetPrediction, Binding Database Home, and TargetNet, the main active components of GPs and their action targets were screened. Disease-related targets were obtained from the GeneCards database. After obtaining the intersection targets, Cytoscape 3.9.0 software was used to construct a network of drug, target, and diseases to screen core targets. Thirty-eight ApoE-/- mice were fed a high-fat diet to establish liver lipid deposition models of MAFLD mice. After successful modeling, they were randomly divided into a model group, a low-dose GPs (GPs-L) group, a high-dose GPs (GPs-H) group, and a simvastatin group. Eight C57BL/6J mice were used as the blank control group, which was given normal feed. The mice in the remaining groups were fed with high-fat feed for 12 weeks. Starting from the ninth week, the mice in the GPs-L group and the GPs-H group were gavaged with GPs at 1.49 g·kg-1·d-1 and 2.97 g·kg-1·d-1, respectively. The mice in the simvastatin group were gavaged with simvastatin at 2.275 mg·kg-1·d-1, and those in the blank control group and the model group were gavaged with the same volume of normal saline for a total of four weeks. The fully automatic biochemical analyzer was used to detect triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) in the serum of mice. Hematoxylin-eosin (HE) staining was used to observe the pathological morphological changes of the liver in mice, and oil red O staining was used to observe the lipid deposition in the liver of mice. Enzyme-linked immunosorbent assay (ELISA) was used to detect the contents of TG and non-esterified fatty acid (NEFA) in the livers of mice in each group. The protein expression level of sirtuin (SIRT6) was detected by immunohistochemistry. The SIRT6/cAMP-response element binding protein (CREB)/orphan nuclear receptor 77 (Nur77) signaling pathway, apoptosis-related mRNA, and protein levels were analyzed by real-time polymerase chain reaction (Real-time PCR) and the Wes automated Western blot system. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was employed to detect cell apoptosis.ResultsA total of 138 potential target genes of the main active components of GPs, such as ginsenoside Rb1, ginsenoside Rb3, ginsenoside Rd, ginsenoside Rg3, ginsenoside compound K, and gypenoside XLIX, are screened. There are 11 134 MAFLD-related targets, with 120 common targets identified, among which SIRT6 is the core target. Molecular docking results show that the above active components have a strong binding affinity with SIRT6. Compared with those in the blank control group, the levels of TC, TG, and LDL-C in the model group are significantly increased, and the level of HDL-C is significantly decreased (P<0.01). The levels of aspartate transferase (AST) and alanine aminotransferase (ALT) in the liver are increased (P<0.01). There are a large number of fat vacuoles in hepatocytes, and orange-red lipid droplets are diffusely distributed, with obvious lipid deposition in the liver. The contents of TG and NEFA are increased (P<0.01). The protein and mRNA expressions of SIRT6, CREB, phosphorylated(p)-CREB, Nur77, and B-cell lymphoma 2 (Bcl-2) are decreased, while the protein expressions of Bcl-2-associated X protein(Bax),cysteine-aspartic protease-9(Caspase-9),Caspase-3, cleaved-Caspase-3 and cleaved-Caspase-9, as well as the mRNA expressions of Bax, Caspase-9, and Caspase-3 are increased (P<0.05, P<0.01). Extensive hepatocyte apoptosis is observed. Compared with those in the model group, after intervention with different doses of GPs and simvastatin, the levels of TC, TG, and LDL-C of mice in the GPs group and simvastatin group are significantly decreased, and the level of HDL-C is significantly increased (P<0.01). The contents of AST and ALT in the liver are decreased (P<0.01). The morphology of hepatocytes tends to be normal, with a decrease in vacuoles and lipid droplets, and the lipid deposition in the liver is alleviated. The contents of TG and NEFA are decreased significantly (P<0.01). The protein and mRNA expressions of SIRT6, CREB, p-CREB, Nur77, and Bcl-2 are increased, while the protein expressions of Bax,Caspase-9,Caspase-3, cleaved-Caspase-3 and cleaved-Caspase-9, as well as the mRNA expressions of Bax, Caspase-9, and Caspase-3 are decreased (P<0.05, P<0.01). The condition of hepatocyte apoptosis shows significant improvement, and the intervention effect of high-dose administration is particularly significant.ConclusionGPs can improve lipid deposition in the liver of MAFLD mice, which is associated with the regulation of the SIRT6/CREB/Nur77 signaling pathway and subsequent effects on cell apoptosis.  
      关键词:gypenoside;metabolic-associated fatty liver disease;sirtuin (SIRT6)/cAMP-response element binding protein (CREB)/orphan nuclear receptor 77 (Nur77) signaling pathway;apoptosis   
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    • ZHU Jingxuan, SONG Nan, LIU Yu, DONG Yuanguang, JIA Lianqun, PEI Yupeng
      Vol. 32, Issue 15, Pages: 45-56(2026) DOI: 10.13422/j.cnki.syfjx.20251612
      摘要:ObjectiveTo investigate whether Ditantang (DTT) improves oleic acid (OA)-induced hepatic lipid accumulation by regulating apoptosis/pyroptosis pathways mediated by apoptosis-related protein activator 1 (Apaf1) sensing the mitochondrial permeability transition (MPT).MethodsHepG2 cells were treated with 800 μmol·L-1 OA to establish a hepatocyte lipid accumulation model. The optimal intervention conditions for DTT-containing serum and the Apaf1 inhibitor ZYZ488 were screened using the cell counting kit-8 (CCK-8) assay. HepG2 cells were divided into the following groups: NC group, OA group (800 µmol·L-1), OA (800 µmol·L-1) + serum control (SC, 10%) group, OA (800 µmol·L-1) + DTT-containing serum (10%) group, and OA (800 µmol·L-1) + ZYZ488 (1 µmol·L-1) group. Hepatic lipid accumulation was evaluated by Oil Red O staining and measurement of triglyceride (TG) and non-esterified fatty acid (NEFA) levels. Calcein-AM and JC-1 fluorescence staining were used to assess MPTP opening and mitochondrial membrane potential alterations. Flow cytometry was performed to determine apoptotic and pyroptotic cell numbers. Real-time PCR was used to detect mRNA expression of Apaf1, gasdermin E (GSDME), poly(ADP-ribose) polymerase 1 (PARP1), Caspase-3, Caspase-4, and Caspase-9. Immunofluorescence analysis was used to assess Apaf1 expression. Western blot analysis was performed to evaluate protein expression of Apaf1, GSDME, PARP1, Caspase-3, Caspase-4, Caspase-9, cleaved Caspase-3, and cleaved Caspase-9.ResultsDTT-containing serum significantly reduced TG and NEFA levels in OA-induced HepG2 cells (P<0.01) and effectively mitigated intracellular lipid droplet accumulation. DTT-containing serum inhibited excessive MPT opening and mitochondrial membrane potential decline (P<0.01). Meanwhile, DTT-containing serum downregulated key genes and proteins in Apaf1-mediated apoptosis (Caspase-9/Caspase-3/PARP1) and pyroptosis (Caspase-4/Caspase-3/GSDME) pathways (P<0.05), with effects comparable to those of ZYZ488.ConclusionDTT improves hepatic lipid accumulation by inhibiting Apaf1-sensed MPT-mediated apoptosis and pyroptosis pathways.  
      关键词:lipid deposition in hepatocytes;Ditantang;apoptosis-related protein activator 1 (Apaf1);mitochondrial permeability transition (MPT);apoptosis;pyroptosis   
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    • DONG Ai, BAI Yunfeng, LI Chenglin, TANG Yanan, WANG Chunguo, XU Yantong
      Vol. 32, Issue 15, Pages: 57-66(2026) DOI: 10.13422/j.cnki.syfjx.20260566
      摘要:ObjectiveTo investigate the antidepressant mechanism of Kaixin San(KXS) by determining the alterations in the fecal metabolome and the 5-hydroxytryptamine(5-HT) system in the gut-brain axis.MethodsThe antidepressant efficacy of KXS was evaluated via the chronic restraint stress(CRS) model. ICR mice were assigned into six groups: control, model, fluoxetine(0.01 g·kg-1), and low-, medium-, and high-dose(2.5, 5.0, 10.0 g·kg-1, respectively) KXS groups. Except the control group, the other groups were subjected to restraint stress for 28 consecutive days while simultaneously receiving preventive gavage of test drugs. Antidepressant effects were assessed by the sucrose preference test(SPT), forced swimming test(FST), tail suspension test(TST), and open field test(OFT). The fecal metabolome of mice was analyzed by UPLC-LTQ-Orbitrap MS, which examined changes in metabolic profiles, differential metabolites, and associated metabolic pathways after KXS treatment. The 5-HT levels in the serum, colon, and cerebral cortex were measured by the enzyme-linked immunosorbent assay(ELISA). Western blot was used to determine the expression of tryptophan hydroxylase (TPH) 1 in the colon and TPH2 in the prefrontal cortex, monoamine oxidase A(MAOA) and serotonin transporter(SERT) in both colon and prefrontal cortex, as well as 5-HT receptor 4(5-HTR4) in the colon and 5-HT receptor 2A(5-HTR2A) in the prefrontal cortex.ResultsCompared with the control group, the model group showed a decreased sucrose preference rate(P<0.01) and increased immobility time in both the FST and TST(P<0.05, P<0.01). Compared with the model group, the medium- and high-dose KXS groups exhibited increased sucrose preference rates(P<0.05, P<0.01) and reduced the immobility time in FST(P<0.01). KXS at all doses significantly decreased the immobility time in TST(P<0.01). Fecal metabolomics analysis identified 7 differential metabolites between the KXS groups and the model group. Metabolic pathway enrichment analysis identified 25 pathways, such as linoleic acid oxylipin metabolism. Kyoto Encyclopedia of Genes and Genomes(KEGG) enrichment further identified two pathways: tryptophan metabolism and steroid biosynthesis. Serum 5-HT levels were decreased in the model group and the low-dose KXS group compared with the control group(P<0.05). Compared with the model group, the medium- and high-dose KXS groups showed an increasing trend of serum 5-HT level but did not reach statistical significance. Compared with the control group, the model group exhibited downregulated expression of TPH1, SERT, 5-HTR4, MAOA as well as a declined 5-HT level in the colon(P<0.05, P<0.01). Compared with the model group, KXS at all the doses upregulated TPH1 and SERT expression(P<0.05, P<0.01), and high-dose KXS increased the 5-HT content(P<0.05) in the colon. Compared with the control group, the model group exhibited downregulated TPH2 and MAOA expression and reduced 5-HT content(P<0.05) and upregulated SERT and 5-HTR2A expression(P<0.01) in the prefrontal cortex. Compared with the model group, KXS at all doses upregulated TPH2 and MAOA expression and 5-HT content(P<0.01) and downregulated SERT and 5-HTR2A expression(P<0.05, P<0.01) in the prefrontal cortex.ConclusionKXS significantly ameliorated depression-like behaviors in mice subjected to CRS by regulating the fecal metabolome and the 5-HT system in the gut-brain axis.  
      关键词:Kaixin San;antidepressant;fecal metabolome;gut-brain axis;5-hydroxytryptamine(5-HT) system   
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    • QIAN Yuhao, BU Xianzhong, GUO Xiaohui, LI Hanxi, WANG Yixin, WANG Ziqi, BU Baoxian
      Vol. 32, Issue 15, Pages: 67-78(2026) DOI: 10.13422/j.cnki.syfjx.20252391
      摘要:ObjectiveTo investigate the effects of Buyang Huanwutang (BYHWD) on ferroptosis-related proteins after spinal cord injury (SCI) through nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway-mediated ferroptosis, and to elucidate the molecular mechanisms underlying the protective effects of BYHWD against SCI.MethodsNinety-six SPF male rats were randomly assigned to a sham-operated group, model group, sulforaphane (SFN) group, and BYHWD group. Except for the sham-operated group, the SCI model at the T9-T10 segment was established using the modified Allen's method. The sham-operated and model groups received normal saline (15 mL·kg-1·d-1) by gavage, the BYHWD group received BYHWD decoction (14.9 g·kg-1·d-1) by gavage, and the SFN group received intraperitoneal injection of SFN (50 mg·kg-1·d-1). Following successful model establishment, the corresponding treatments were administered for 7 or 14 days. After SCI induction and after 7 and 14 days of intervention, Basso Beattie Bresnahan (BBB) locomotor scoring, inclined plane testing, hematoxylin-eosin (HE) staining, immunohistochemistry (IHC), enzyme-linked immunosorbent assay (ELISA), Western blot, and real-time polymerase chain reaction (Real-time PCR) were performed to evaluate hindlimb motor function, morphological changes of neurons in the anterior horn of the spinal cord, and the expression of proteins and genes involved in the Nrf2/HO-1 ferroptosis signaling pathway.Results① Compared with the sham-operated group, the model groups showed significantly decreased BBB locomotor scores and inclined plane angles after 7 and 14 days of intervention (P<0.05). Cellular structures were disrupted, nuclei were pyknotic, and most nucleoli and nuclear membranes disappeared. Tissue architecture became disorganized, spinal cord cavities increased, and inflammatory cell infiltration was severe. The numbers of GAP-43- and NF200-positive cells were significantly reduced (P<0.05). Iron ion and malondialdehyde (MDA) levels were significantly increased (P<0.01), whereas glutathione peroxidase 4 (GPX4), glutathione (GSH), superoxide dismutase (SOD), and the protein and mRNA expression levels of Nrf2 and HO-1 were significantly decreased (P<0.01). ② Compared with the model group, the SFN and BYHWD groups exhibited significantly increased BBB locomotor scores and inclined plane angles at both time points (P<0.01). In both groups, cellular structures were relatively intact, neuronal swelling was alleviated, and tissue cavitation and cell necrosis were reduced. The numbers of GAP-43- and NF200-positive cells were significantly increased (P<0.05). After 7 days of intervention, the SFN group showed significantly reduced iron ion levels and increased GPX4 levels (P<0.01), accompanied by significantly increased protein and mRNA expression of Nrf2 and HO-1 (P<0.05,P<0.01). In the BYHWD group, changes in iron ion and GPX4 levels were not statistically significant. The protein expression of Nrf2 and HO-1 and the mRNA expression of Nrf2 also showed no significant differences, whereas HO-1 mRNA expression was significantly upregulated (P<0.05). After 14 days of intervention, both groups exhibited significantly decreased iron ion and MDA levels (P<0.01), significantly increased GPX4, GSH, and SOD levels (P<0.01), and significantly elevated protein and mRNA expression of Nrf2 and HO-1 (P<0.01). ③ Compared with the SFN group, the BYHWD group showed no significant differences in BBB locomotor scores or inclined plane angles at either time point. Most neuronal intercellular spaces appeared normal, with only a small number of neurons exhibiting irregular morphology, relatively intact structures, and mild swelling. Tissue cavitation and cell necrosis were reduced. No significant differences were observed between the two groups in the numbers of GAP-43- and NF200-positive cells or in the levels of iron ions, GPX4, GSH, SOD, and MDA at either time point. After 7 days of intervention, no significant difference was found in Nrf2 protein expression, whereas HO-1 protein expression was significantly downregulated (P<0.05). After 14 days of intervention, the protein expression of both Nrf2 and HO-1 was significantly downregulated (P<0.05). Similarly, no significant difference was observed in Nrf2 mRNA expression after 7 days of intervention, whereas HO-1 mRNA expression after 7 days and Nrf2 and HO-1 mRNA expression after 14 days were significantly downregulated (P<0.05).ConclusionBYHWD can regulate the Nrf2/HO-1 signaling pathway and inhibit ferroptosis after SCI. It contributes to the improvement of hindlimb motor dysfunction and promotes axonal regeneration of spinal neurons after SCI, which may represent one of the mechanisms underlying its protective effects against SCI.  
      关键词:spinal cord injury;ferroptosis;Buyang Huanwutang;nuclear factor E2-related factor 2;heme oxygenase-1   
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    • YANG Huan, LU Yujie, LIANG Wei, LIU Zhilong, HE Xinying, SUN Xinyu, WU Chao, LI Meng, SUN Yunchuan
      Vol. 32, Issue 15, Pages: 79-89(2026) DOI: 10.13422/j.cnki.syfjx.20251801
      摘要:ObjectiveTo investigate the effects and mechanisms of Anchang group prescription on radiation enteritis (RE) based on the phosphatidylinositol 3-kinase/protein kinase B-glycogen synthase kinase 3β (PI3K/Akt-GSK3β) pathway by observing the expression levels of key regulatory factors in mice after radiotherapy.MethodsEighty-six mice were randomly divided into two groups: a normal group (n=14) and a radiation group (n=72). The RE model was established in the radiation group through a single abdominal irradiation of 15 Gray (Gy). Following successful model establishment, the radiation group was further divided into five groups (n=14 each): the model group, the low-, medium-, and high-dose Anchang group prescription groups (11.89, 23.79, 47.57 g·kg-1, respectively), and the glutamine group (0.80 g·kg-1). Each group received consecutive gavage treatment for 7 d, during which the basic condition of the mice was monitored and the disease activity index (DAI) was recorded. After the administration, the mice were euthanized, and the colon length was measured. Hematoxylin-eosin/Masson trichrome (HE/Masson) staining was performed, and the colonic mucosal damage index (CMDI) was evaluated. Enzyme-linked immunosorbent assay (ELISA) was used to examine the levels of colonic oxidative stress indicators, including reactive oxygen species (ROS), glutathione (GSH), and malondialdehyde (MDA), as well as the content of serum inflammatory cytokines: interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). Western blot was conducted to detect the expression changes of the aforementioned inflammatory cytokines, zonula occludens-1 (ZO-1), Claudin-1, acyl-CoA synthetase long-chain family member 4 (ACSL4), ferritin heavy chain 1 (FTH1), and glutathione peroxidase 4 (GPX4), as well as proteins related to the PI3K/Akt-GSK3β signaling pathway in colon tissue.ResultsCompared with those in the normal group, mice in the model group generally exhibited poorer condition with weight loss and shortened colon length (P<0.05). Colon tissue showed crypt destruction, goblet cell loss, and inflammatory infiltration. DAI and CMDI scores, as well as serum IL-1β, IL-6, and TNF-α levels, were elevated (P<0.05). Colon tissue also exhibited increased ROS and MDA levels and a decreased GSH level (P<0.05). The protein expression levels of ZO-1, Claudin-1, GPX4, FTH1, phosphorylated(p)-PI3K, p-Akt, and p-GSK3β were decreased, while that of ACSL4 was elevated (P<0.05). After intervention with the Anchang group prescription, the above indicators showed dose-dependent improvement compared with those in the model group: general condition significantly improved, weight loss trend was alleviated, and colon length was restored. Histopathological examination of the colon tissue revealed crypt structure reconstruction, increased goblet cells, and reduced fibrosis area. DAI and CMDI scores as well as the levels of serum inflammatory cytokines decreased (P<0.05). The levels of ROS and MDA decreased, while that of GSH increased (P<0.05). The protein expression levels of ZO-1, Claudin-1, GPX4, FTH1, p-PI3K, p-Akt, and p-GSK3β increased, while that of ACSL4 decreased (P<0.05). In addition, the high-dose group exhibited the strongest effect, with the efficacy of the glutamine group being comparable to that of the high-dose group.ConclusionThe Anchang group prescription can enhance antioxidant capacity by activating the PI3K/Akt-GSK3β signaling pathway, thereby inhibiting ferroptosis in intestinal cells, promoting the repair of intestinal mucosal barrier function, and ultimately improving radiation-induced intestinal injury.  
      关键词:radiation enteritis;Anchang group prescription;oxidative stress;ferroptosis;intestinal injury   
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    • WU Tong, ZHANG Anni, LI Le, ZHANG Changxi
      Vol. 32, Issue 15, Pages: 90-100(2026) DOI: 10.13422/j.cnki.syfjx.20260466
      摘要:ObjectiveThis paper aims to explore the mechanism of action of Shengjiang Pingchuan Zhike pills (SPZP) in improving bronchial asthma (AS) via regulating apoptosis mediated by endoplasmic reticulum stress based on transcriptomics and conduct experimental verification.MethodsSixty SD rats were randomly divided into a blank group, a model group, a positive drug group (dexamethasone injection, 0.125 mg·kg-1), and low-, medium-, and high-dose SPZP groups (540, 1 080, 2 160 mg·kg-1), with 10 rats in each group. An AS model was established by intraperitoneally injecting the mixed solution of ovalbumin and aluminum hydroxide combined with nebulization challenge. After successful modeling, the rats were intervened for 21 days and then sacrificed for sample collection. The pathological changes of lung tissue were observed by hematoxylin-eosin (HE) staining. The serum immunoglobulin E (IgE) levels of rats were detected by enzyme-linked immunosorbent assay (ELISA). The ultrastructure of endoplasmic reticulum and apoptosis was observed by transmission electron microscope (TEM). The molecular mechanism of SPZP intervention in AS was explored by RNA-sequencing (RNA-seq) analysis of rats' lung tissue. The apoptosis rate was detected by in situ terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The protein expression levels of C/EBP homologous protein (CHOP), B-cell lymphoma-2 associated X protein (Bax), and B-cell lymphoma-2 (Bcl-2) in lung tissue were detected by Western blot. Human bronchial epithelial cells (BEAS-2B) were induced by lipopolysaccharide to establish injury models, which were divided into a blank group, a model group, and low-, medium-, and high-dose SPZP-containing serum groups. The cell morphology was observed by cell imaging microscope. The ultrastructure of endoplasmic reticulum was observed by TEM. The apoptosis rate was detected by flow cytometry, and the nuclear aggregation of CHOP protein was observed by immunofluorescence (IF). The mRNA expression of endoplasmic reticulum-related glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), Bax, and Bcl-2 in cells was detected by real-time fluorescence quantitative polymerase chain reaction (Real-time PCR). The protein expression of GRP78, CHOP, ATF6, Bax, Bcl-2, and cleaved Caspase-3 in cells was detected by Western blot.ResultsAnimal experiments show that compared with those in the blank group, the rats in the model group present frequent wheezing with stridor, coughing, reduced activity, rapid breathing frequency, and other symptoms. In the lung tissue pathology, the airway epithelium of the rats in the model group was shed, and inflammatory cells were infiltrated. The airway wall was thickened. In the ultrastructure, the endoplasmic reticulum was dilated, and chromatin was condensed. The cell nucleus was pyknotic. The serum IgE level was increased (P<0.01), while the SPZP intervention group could improve the above results (P<0.01). RNA-seq analysis shows that there are 515 differentially expressed genes in the blank group and the model group and 1 852 differentially expressed genes in the model group and the high-dose group. 74 differentially expressed intersection genes were significantly enriched in asthma, apoptosis, and endoplasmic reticulum protein processing pathways. TUNEL staining and Western blot shows that compared with the blank group, the apoptosis rate of lung tissue cells is significantly increased (P<0.01), the protein expression of CHOP and Bax is significantly upregulated (P<0.01), while Bcl-2 is significantly downregulated (P<0.01) in the model group. The SPZP intervention group significantly improved the above detected indicators (P<0.01). Cell experiments results show that SPZP-containing serum dose-dependently increases the survival rate of BEAS-2B cells (P<0.01) and improves the disorder of cell morphology, chromatin condensation, and endoplasmic reticulum swelling and rupture. The apoptosis rate was significantly decreased as shown by flow cytometry (P<0.01). The expression of GRP78, ATF6, and Bax mRNA, as well as that of GRP78, CHOP, ATF6, Bax, and cleaved caspase-3 proteins were downregulated (P<0.05, P<0.01), while the expression of Bcl-2 mRNA and Bcl-2 protein was upregulated (P<0.05, P<0.01).ConclusionIn vivo and in vitro experiments confirm that the intervention of SPZP in AS may be related to the regulation of the excessive activation of the GRP78/ATF6/CHOP signaling pathway and the alleviation of epithelial cell apoptosis mediated by endoplasmic reticulum stress.  
      关键词:bronchial asthma;Shengjiang Pingchuan Zhike pills;transcriptomics;endoplasmic reticulum stress;epithelial cell apoptosis   
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    • LI Yu, CAI Qingqing, YAN Jing, ZHANG Fangbo, TANG Shihuan
      Vol. 32, Issue 15, Pages: 101-109(2026) DOI: 10.13422/j.cnki.syfjx.20252342
      摘要:ObjectiveThis paper aims to explore the mechanism of action of Zhishe Tongluo capsules in intervening ischemic stroke by regulating the adenosine monophosphate-activated protein kinase (AMPK)/UNC-51-like kinase 1 (ULK1)/homologue of yeast autophagy-related gene 6 (Beclin1) signaling pathway.MethodsMale Sprague-Dawley (SD) rats were randomly divided into a sham group, a model group, Zhishe Tongluo capsule groups with low, medium, and high doses (0.63, 1.25, 2.50 g·kg-1), and the Ginaton group (25 mg·kg-1). A middle cerebral artery occlusion (MCAO) rat model was established using the modified intraluminal suture occlusion method. All treatments were administered continuously for seven days after modeling. Brain injury was evaluated using 2,3,5-triphenyltetrazolium chloride (TTC) staining, neurobehavioral scores, hematoxylin-eosin (HE) staining, and Nissl staining. The expression levels of AMPK, ULK1, Beclin1, and B-cell lymphoma-2 (Bcl-2)/E1B 19 kDa-interacting protein 3-like protein (BNIP3L) in brain tissue were detected by both immunohistochemistry (IHC) and Western blot. Additionally, an oxygen-glucose deprivation (OGD)-induced injury model was constructed in rats’ adrenal medullary pheochromocytoma cells (PC12). The expression levels of Beclin1 and BNIP3L in the cells were detected by Western blot.ResultsAnimal experimental results show that, compared with the sham group, the model group exhibits significantly increased rats' neurobehavioral scores and cerebral infarction area (P<0.01), significantly increased number of abnormal neurons (P<0.01), significantly reduced number of Nissl bodies (P<0.01), and significantly upregulated expression levels of AMPK, ULK1, Beclin1, and BNIP3L (P<0.05,P<0.01). After treatment with Zhishe Tongluo capsules, compared with the model group, the Zhishe Tongluo capsule group with high dose and the Ginaton group exhibited significantly reduced neurobehavioral scores and cerebral infarction area (P<0.05,P<0.01). Zhishe Tongluo capsules groups with medium and high doses and the Ginaton group exhibited significantly decreased number of abnormal neurons (P<0.05,P<0.01). Zhishe Tongluo capsule groups with different doses and the Ginaton group exhibited significantly increased number of Nissl bodies (P<0.05,P<0.01), and the expression levels of AMPK, ULK1, Beclin1, and BNIP3L were significantly downregulated (P<0.05). Cellular experimental results show that, compared with the normal group, the expression levels of Beclin1 and BNIP3L in OGD-induced PC12 cells were significantly increased (P<0.01). Compared with the OGD group, the expression levels of Beclin1 and BNIP3L were significantly decreased in the intestinal absorption liquid group of high-dose Zhishe Tongluo capsules and the edaravone group (P<0.05).ConclusionZhishe Tongluo capsules exert neuroprotective effects by regulating the AMPK/ULK1/Beclin1 signaling pathway, thereby alleviating cerebral ischemic injury.  
      关键词:ischemia stroke;oxygen-glucose deprivation;Zhishe Tongluo capsules;adenosine monophosphate-activated protein kinase (AMPK)/UNC-51-like kinase 1 (ULK1)/homologue of yeast autophagy-related gene 6 (Beclin1) signaling pathway;mechanism of action   
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    • ZHU Xinhua, HE Menghao, ZENG Yang, FU Xinying, YAO Xinyan, LIU Kan
      Vol. 32, Issue 15, Pages: 110-122(2026) DOI: 10.13422/j.cnki.syfjx.20252240
      摘要:ObjectiveThis paper aims to investigate the improving effects of Huangqi Chongteng Yin (HQCTY) against the no-reflow phenomenon in the middle cerebral artery occlusion/reperfusion (MCAO/R) mouse model and to elucidate its potential mechanisms.MethodsA modified intraluminal filament method was used to establish the MCAO/R models in C57BL/6 mice. The models were assigned into a sham group, a model group, HQCTY groups with low dose (6.63 g·kg-1), medium dose (13.26 g·kg-1), and high dose (26.52 g·kg-1), and a 3-n-butylphthalide positive group (78 mg·kg-1), with 15 mice in each group. All drugs were administered once daily by intragastric gavage for seven consecutive days. Neurological deficits were assessed using the modified neurological severity score (mNSS). Laser speckle contrast imaging (LSCI) was used to evaluate the no-reflow phenomenon in ischemia-reperfusion. 2,3,5-triphenyltetrazolium chloride (TTC) staining was performed to measure the volume of ischemic infarct and cerebral edema. Hematoxylin-eosin (HE) staining, Nissl staining, silver staining, and Fluoro-Jade B (FJB) staining were used to observe histopathological changes and neuronal damage in the neural tissues. Evans blue staining together with immunofluorescent detection of tight junction proteins zonula occludens-1 (ZO-1) and Claudin-5 was used to evaluate blood-brain barrier (BBB) function. Platelet endothelial cell adhesion molecule-1 (CD31)/vascular endothelial growth factor (VEGF) immunofluorescent staining was performed to assess angiogenesis and microcirculatory perfusion. Immunofluorescence was performed to detect phosphorylated (p)- receptor-interacting serine/threonine-protein kinase 1 (RIPK)-3/p-mixed lineage kinase domain-like protein (MLKL). Combined with Western blot, the immunofluorescent staining was used to detect RIPK1, RIPK3, MLKL, and their phosphorylated forms, evaluating the necroptotic signaling pathway. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interleukin-18 (IL-18)ResultsCompared with the model group, HQCTY groups with medium and high doses exhibited significantly reduced mNSS scores of MCAO/R mouse model with intragastric administration for three and seven days (P<0.05,P<0.01). LSCI analysis shows that compared with the model group, HQCTY groups with medium and high doses exhibit markedly improved cerebral blood perfusion after reperfusion in the MCAO/R mouse model (P<0.01), thereby alleviating the focal no-reflow phenomenon. TTC staining results reveal that compared with the model group, HQCTY groups with medium and high doses exhibit significantly reduced volume of cerebral ischemic infarct and cerebral edema (P<0.05, P<0.01) in the MCAO/R mouse model. Histopathological evaluation results show that compared with the model group, the HQCTY group with high dose exhibits ordered neuronal arrangement and intact cellular structure (P<0.01) and significantly increased number of Nissl bodies (P<0.01). HQCTY groups with medium and high doses exhibit compact arrangement and distinct orientation of nerve fibers (P<0.01) and markedly reduced neuronal degeneration and necrosis (P<0.01). Compared with the model group, HQCTY groups with medium and high doses exhibited significantly reduced BBB permeability (P<0.01) and increased Claudin-5 and ZO-1 expression (P<0.01) in the no-reflow region of the MCAO/R mouse model. Compared with the model group, HQCTY groups with medium and high doses exhibited significantly increased microvessel density and upregulated VEGF expression in the no-reflow region of the MCAO/R mouse model (P<0.05,P<0.01). Immunofluorescence and Western blot assays demonstrate that compared with the model group, HQCTY groups with medium and high doses exhibit significantly downregulated protein expression of p-RIPK1, p-RIPK3, and p-MLKL in the no-reflow region of the MCAO/R mouse model (P<0.05, P<0.01). Compared with the model group, HQCTY groups with medium and high doses exhibited significantly downregulated levels of IL-1β, IL-6, TNF-α, and IL-18 in the no-reflow region of the MCAO/R mouse model (P<0.01).ConclusionHQCTY may regulate the RIPK1/RIPK3/MLKL signaling pathway, inhibiting necroptosis, enhancing cerebral microcirculatory perfusion and acting on multiple targets to improve the no-reflow phenomenon and associated neuronal damage following cerebral ischemia-reperfusion. These findings indicate its promising neuroprotective potential and application prospects.  
      关键词:cerebral ischemia-reperfusion;no-reflow phenomenon;Huangqi Chongteng Yin;blood-brain barrier;necroptosis   
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    • DENG Chaoyang, XIAO Min, JIANG Xiaocui, WANG Chaoyang, LYU Yinjuan, SHU Jinsong, ZHOU Yanyan, YU Xiaoming
      Vol. 32, Issue 15, Pages: 123-132(2026) DOI: 10.13422/j.cnki.syfjx.20252409
      摘要:ObjectiveTo study the effect and mechanism of Shugan Bushen Yulin decoction in enhancing sperm motility in rats with liver Qi stagnation based on acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated mitochondrial fatty acid β-oxidation.MethodsForty male SD rats were divided into the normal control group, the model group, the high-dose (26 g·kg-1) Shugan Bushen Yulin decoction treatment group, the low-dose (13 g·kg-1) Shugan Bushen Yulin decoction treatment group, and the fluoxetine (1.8 mg·kg-1) treatment group by using a random number table. All the administration groups were administered by gavage. Except for the normal control group, the rat models of liver Qi stagnation in other groups were replicated by chronic restraint combined with irritation by tail nipping. After the modeling was completed, each group was administered the corresponding drug for 21 consecutive days. Enzyme-linked immunosorbent assay (ELISA) was used to detect corticosterone (CORT), testosterone (T), and estradiol (E2) in the serum of rats with liver depression. The body weight and testicular and epididymal mass of rats were determined using an electronic analytical balance, and the testis index and epididymis index were calculated accordingly. Sperm concentration and sperm motility were determined using an automatic sperm analysis system. Hematoxylin-eosin (HE) staining was used for histological observation of testicular tissue to evaluate its pathological morphological changes. The membrane potential level of sperm mitochondria was analyzed using flow cytometry with the aid of fluorescent probes such as JC-1. Liquid chromatography-mass spectrometry (LC-MS) was used to detect changes in sperm lipid metabolism and screen for metabolic differences. The activities of acetyl-CoA and acyl-CoA and the content of adenosine triphosphate (ATP) were detected by ELISA. The expression of ACSL4 in testicular tissue was detected by immunofluorescence. The expression levels of ACSL4 and carnitine palmitoyltransferase 1 (CPT1) proteins in testicular tissue were detected by Western blot.ResultsLC-MS screened out 24 differential fatty acid metabolites in comparison with the normal control group. After intervention with Shugan Bushen Yulin decoction, 11 differential fatty acid metabolites were upregulated. Pathway enrichment analysis revealed that they were mainly involved in fatty acid biosynthesis and fatty acid metabolism. Compared with those in the normal control group, the sperm density and motility, epididymis index, and mitochondrial membrane potential of rats in the model group decreased significantly, the activities of acetyl-CoA and acyl-CoA and the ATP content decreased, and the protein expression of ACSL4 and CPT1 decreased (P<0.01). Compared with the model group, low- and high-dose Shugan Bushen Yulin decoction treatment groups showed improved perm density and motility, epididymis index, and mitochondrial membrane potential of rats (P<0.01), elevated activities of acetyl-CoA and acyl-CoA and ATP content (P<0.01), and upregulated ACSL4 and CPT1 protein expression (P<0.05, P<0.01).ConclusionShugan Bushen Yulin decoction can improve sperm motility in rats with liver Qi stagnation by activating ACSL4-mediated mitochondrial fatty acid β-oxidation and enhancing ATP production.  
      关键词:Shugan Bushen Yulin decoction;lemotions;liver Qi stagnation;sperm motility;mitochondria;fatty acid β-oxidation   
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    • ZHANG Shaowen, YI Tao, SU Yao, QIN Zhijun, LEI Ting, TANG Yizuo, LI Hanquan, QIU Feng, ZHOU Ziyang, ZENG Xianxiang, XIANG Yun, ZHANG Xiuli
      Vol. 32, Issue 15, Pages: 133-142(2026) DOI: 10.13422/j.cnki.syfjx.20260544
      摘要:ObjectiveThis paper aims to investigate whether Baihuan Xiaoyao decoction alleviates depressive-like behaviors induced by chronic unpredictable mild stress (CUMS) by activating rats' hippocampal σ-1 receptors (σ-1R).MethodsSixty Sprague-Dawley (SD) rats, aged three weeks, were allocated randomly into a normal group, a CUMS model group, a positive drug group (fluoxetine, 0.002 g·kg-1·d-1), and Baihuan Xiaoyao decoction groups with low (5.36 g·kg-1·d-1), medium (10.71 g·kg-1·d-1), and high (21.42 g·kg-1·d-1) doses, with 10 rats in each group. The depression model was established using CUMS, followed by 28 days of drug intervention. The open field test (OFT) was used to assess spontaneous locomotor activity, exploratory behavior, and anxiety of rats. The sucrose preference test (SPT) was employed to evaluate the degree of anhedonia. The forced swim test (FST) was used to assess despair behavior, and the Morris water maze (MWM) test was employed to evaluate spatial learning and memory capability. Hematoxylin-eosin (HE) staining was performed to assess hippocampal damage, and transmission electron microscope (TEM) was used to observe morphological changes in the endoplasmic reticulum. Western blot and immunofluorescence were employed to detect the protein expression levels of σ-1R, binding immunoglobulin protein (BiP) in the endoplasmic reticulum, inositol-requiring enzyme 1α (IRE1α), phosphorylated (p)-IRE1α, X-box binding protein 1 (XBP1), pro-apoptotic transcription factor C/EBP homologous protein (CHOP), B-cell lymphoma-2 (Bcl-2), and Bcl-2-associated X protein (Bax).ResultsBehavioral assessments show that compared with the normal group, the CUMS model group exhibits significant anhedonia, behavioral despair, reduced exploratory behavior, and spatial memory impairment (decreased sucrose preference rate, prolonged immobility time in the FST, reduced central distance in the OFT, and extended escape latency, P<0.05, P<0.01). Compared with the CUMS model group, the Baihuan Xiaoyao decoction groups with medium and high doses exhibited significantly improved behavioral parameters (P<0.05, P<0.01). Morphological observations reveal that compared with the normal group, the CUMS model group shows disordered neuronal arrangement and increased intercellular space in the rats' hippocampal CA1 and DG regions, along with marked endoplasmic reticulum dilation and degranulation. Compared with the CUMS model group, the Baihuan Xiaoyao decoction group with high dose markedly alleviated these pathological changes, with neuronal arrangement becoming more regular and endoplasmic reticulum morphology and quantity nearly restored to normal levels. Western blot and immunofluorescence analyses demonstrate that compared with the normal group, the CUMS model group exhibits significantly decreased σ-1R protein and anti-apoptotic protein Bcl-2 expression (P<0.01) and significantly increased expression of endoplasmic reticulum stress-related proteins BiP, p-IRE1α, XBP1, CHOP, and Bax in the rats' hippocampal tissue (P<0.01). Compared with the CUMS model group, Baihuan Xiaoyao decoction groups with the medium and high doses exhibited significantly upregulated σ-1R and Bcl-2 expression (P<0.01), as well as significantly downregulated expression of BiP, p-IRE1α, XBP1, CHOP, and Bax (P<0.01).ConclusionBaihuan Xiaoyao decoction may exert its antidepressant effects by activating hippocampal σ-1R and inhibiting the endoplasmic reticulum stress and apoptotic pathway. This study provides a modern pharmacological basis for the clinical application of Baihuan Xiaoyao decoction in traditional Chinese medicine and offers new targets and insights for treating adolescent depression with Chinese herbal medicine.  
      关键词:Baihuan Xiaoyao decoction;adolescent depression;hippocampus;sigma-1 receptor;endoplasmic reticulum stress   
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    • XIONG Mengxin, CHEN Yingqing, ZHANG Haoxue, JIANG Zeyu, XIANG Nan, XU Jun, DENG Ali
      Vol. 32, Issue 15, Pages: 143-152(2026) DOI: 10.13422/j.cnki.syfjx.20252309
      摘要:ObjectiveTo explore the effect of Bushen Huatan prescription on aerobic glycolysis of MC3T3-E1 mouse embryonic osteoblasts based on the hypoxia-inducible factor-1 (HIF-1) signaling pathway and further investigate the mechanism of Bushen Huatan decoction in the intervention of postmenopausal osteoporosis (PMOP).MethodsMC3T3-E1 cells were assigned into blank, low-dose (0.01 g·L-1) Bushen Huatan decoction, medium-dose (0.05 g·L-1) Bushen Huatan prescription, high-dose (0.1 g·L-1) Bushen Huatan prescription, and icaritin (0.1 g·L-1) groups. Alkaline phosphatase (ALP) staining and alizarin red S (ARS) staining were used to determine the osteogenic activity and mineralized nodules of cells in each group. Scanning electron microscopy was employed to observe the ultrastructural changes of mitochondria and rough endoplasmic reticulum in osteoblasts. Immunofluorescence assay was adopted to detect the expression of Runt-related transcription factor 2 (Runx2) and osteogenic-specific transcription factor antibody (Osterix). Enzyme-linked immunosorbent assay was employed to measure the levels of pyruvic acid (PA) and lactic acid (LA) in cell supernatants. The Seahorse XF96 extracellular flow analyzer was used to measure the extracellular acidification rate (ECAR). Western blot and Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) were employed to determine the protein and mRNA levels, respectively of hypoxia-inducible factor-1α (HIF-1α), HIF-1β, pyruvate dehydrogenase kinase isozyme 1 (PDK1), hexokinase 2 (HK2), and M2-type pyruvate kinase isozyme (PKM2).ResultsCompared with the blank group, each treatment group showed increased positive areas of ALP and ARS staining in MC3T3-E1 cells (P<0.05, P<0.01), significantly expanded and increased rough endoplasmic reticula, increased lysosomes, enhanced fluorescence intensities of Runx2 and Osterix (P<0.01), elevated levels of PA and LA in the cell supernatants (P<0.01), increased ECAR within the same time period (P<0.05), and upregulated protein and mRNA levels of HIF-1α, HK2, PDK1, and PKM2 (P<0.05, P<0.01).ConclusionBushen Huatan prescription can regulate aerobic glycolysis in MC3T3-E1 osteoblasts by upregulating the HIF-1 signaling pathway, thereby promoting bone formation.  
      关键词:Bushen Huatan prescription;postmenopausal osteoporosis;osteoblast differentiation;hypoxia-inducible factor-1 (HIF-1) signaling pathway;aerobic glycolysis   
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    • LIN Hongrong, XU Nuo, TANG Xianqin, ZOU Jiayi, ZHONG Zilan, ZHENG Bohui, PAN Wenhao, LIN Chuhua
      Vol. 32, Issue 15, Pages: 153-162(2026) DOI: 10.13422/j.cnki.syfjx.20252305
      摘要:ObjectiveTo investigate the potential active ingredients, key targets, and signaling pathways of Daturae Flos in ameliorating chronic obstructive pulmonary disease (COPD), predict the binding affinity between active ingredients and key targets through molecular docking, and validate the therapeutic efficacy and mechanism through animal experiments, thereby providing experimental evidence for the clinical application of Daturae Flos.MethodsThe active ingredients of Daturae Flos were retrieved from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), and their common targets shared with COPD were identified. Key targets were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Molecular docking was performed to predict binding affinity. For animal experiments, 48 SD rats were randomly assigned into normal control, model control, positive control (ambroxol hydrochloride, 40 mg·kg-1), and low-, medium-, and high-dose (9, 18, 36 mg·kg-1, respectively) Daturae Flos groups. The COPD model was established by intratracheal instillation of lipopolysaccharide (LPS) combined with cigarette smoke exposure. The drugs for intervention were administered by gavage at corresponding doses per day. After 3 weeks of intervention, hematoxylin-eosin (HE) staining was employed to observe the pathological changes in the lung tissue, and Western blot was employed to quantify the expression of related proteins.ResultsA total of 24 active ingredients of Daturae Flos were screened out, with 221 common targets shared with COPD. Key ingredients such as hydroxyphenyl and atropine may exert their effects by regulating targets including protein kinase B1 (Akt1) and epidermal growth factor receptor (EGFR), as well as signaling pathways such as phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt). Animal experiment results showed that compared with the normal control group, the model control group had obvious inflammatory cell infiltration and alveolar structure destruction in the lung tissue, with an increase in mean linear intercept (MLI) (P<0.05), a decrease in mean alveolar number (MAN) (P<0.05), up-regulated protein levels of cleaved cysteinyl aspartate-specific proteinase 3 (cleaved Caspase-3), EGFR, matrix metalloproteinase-9 (MMP-9), α-smooth muscle actin (α-SMA), mucin 5AC (MUC5AC), and non-receptor tyrosine kinase (SRC) (P<0.01), and down-regulated protein level of phosphorylated protein kinase B (p-Akt) (P<0.01). Compared with the model control group, all drug intervention groups showed alleviated pathological damage of the lung tissue, with a decrease in MLI (P<0.05) and an increase in MAN (P<0.05). Medium and high doses of Daturae Flos downregulated the protein levels of cleaved caspase-3, EGFR, MMP-9, α-SMA, MUC5AC, and SRC (P<0.01) and upregulated the protein level of p-Akt (P<0.01).ConclusionDaturae Flos reduces inflammation and oxidative stress in the rat model of COPD by multi-ingredient, multi-target regulation of the PI3K/Akt signaling pathway, thereby ameliorating alveolar damage and delaying the progression of COPD.  
      关键词:Daturae Flos;chronic obstructive pulmonary disease (COPD);network pharmacology;molecular docking;animal experiments   
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    • XU Xiaosong, DU Lipeng, LUO Ziyue, ZHOU Pingping, ZHANG Haiqiang, CHANG Liping, ZHANG Shixiong
      Vol. 32, Issue 15, Pages: 163-170(2026) DOI: 10.13422/j.cnki.syfjx.20252137
      摘要:ObjectiveTo investigate the effects and mechanisms of Cistanches Herba polysaccharides (CHPs) on ameliorating intestinal aging.MethodsForty 20-month-old C57BL/6J mice were randomly assigned to the natural aging group, low-dose CHPs group (2.5 g·kg-1), high-dose CHPs group (5.0 g·kg-1), and β-nicotinamide mononucleotide (NMN) group (200 mg·kg-1). Another 10 2-month-old C57BL/6J mice served as the young control group. All groups received intragastric administration for two months, with the young control and natural aging groups receiving an equal volume of saline (10 mL·kg-1). Senescence-associated β-galactosidase (SA-β-gal) staining was used to assess intestinal senescence. Real-time quantitative polymerase chain reaction (Real-time PCR) detected the mRNA levels of senescence-associated secretory phenotype (SASP) factors, including chemokine (C-X-C motif) ligand 1 (CXCL-1), interleukin-6 (IL-6), matrix metalloproteinase-2 (MMP-2), nuclear factor kappa B (NF-κB), p16, and tumor necrosis factor-alpha (TNF-α) in ileal tissue. Immunofluorescence staining assessed the expression of the tight junction protein Zonula Occludens-1 (ZO-1). Immunohistochemistry evaluated the levels of the proliferation marker Ki67 and the stem cell marker Leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5). Serum lipopolysaccharide (LPS) content was measured by enzyme-linked immunosorbent assay (ELISA). Western blot analyzed the protein levels of inflammasome components NOD-like receptor protein 3 (NLRP3), Caspase-1, and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC). Real-time PCR was performed to determine the mRNA levels of downstream inflammatory cytokines IL-1β and IL-18.ResultsCompared with the young control group, the natural aging group showed increased SA-β-gal-positive cells, upregulation of SASP-related genes (P<0.05, P<0.01), decreased ZO-1 protein (P<0.01), reduced Ki67 and Lgr5 expression (P<0.01), and elevated levels of LPS (P<0.01), NLRP3, Caspase-1, and ASC proteins. Compared with the natural aging group, CHPs treatment significantly ameliorated these aging-related indicators, including reduced SA-β-gal-positive cells, downregulated SASP gene expression (P<0.05, P<0.01), increased ZO-1, Ki67, and Lgr5 levels (P<0.01), and suppressed NLRP3 inflammasome activation and LPS release (P<0.01).ConclusionCHPs ameliorate intestinal aging in naturally aged mice by reducing LPS levels, inhibiting NLRP3 inflammasome activation, downregulating SASP expression, promoting intestinal cell proliferation and stem cell function, and repairing the intestinal barrier.  
      关键词:intestinal aging;inflammation;NOD-like receptor protein 3 (NLRP3) inflammasome;cistanche polysaccharides;traditional Chinese medicine   
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    • CHEN Jiye, HUA Zhen, ZHU Yushuo, XUE Yitao, LI Yunlun
      Vol. 32, Issue 15, Pages: 171-180(2026) DOI: 10.13422/j.cnki.syfjx.20260393
      摘要:Resistant hypertension (RH) is a high-risk cardiovascular disease that has attracted considerable attention in recent years. Owing to the difficulty of blood pressure control and the high risk of target-organ damage, RH poses a major public health challenge and has become one of the key difficulties in modern medical management. Integrated traditional Chinese and Western medicine (TCM-WM) treatment has demonstrated unique comprehensive advantages and considerable potential in improving blood pressure control, effectively alleviating symptoms, and enhancing overall quality of life and long-term prognosis in patients with RH. However, several issues remain unresolved, including the lack of uniform criteria for TCM syndrome differentiation and classification and the challenge of effectively integrating TCM with modern WM treatment strategies. Consequently, a widely recognized and clinically applicable expert consensus has not yet been established. Existing expert consensuses mainly focus on the evidence-based use of Western medications, with limited attention given to the evaluation of the clinical efficacy of TCM and non-pharmacological therapies. As a result, they are unable to fully meet the diagnostic and therapeutic needs associated with the complex clinical manifestations of RH, leading to a lack of standardized guidance for integrated TCM-WM management in clinical practice. To further standardize and optimize the integrated diagnosis and treatment of RH and improve the overall level of TCM-WM management of RH in China, experts in cardiovascular medicine of TCM and WM, and methodology were organized nationwide to develop this consensus. Through a series of procedures, including consensus drafting, expert interviews, and evidence synthesis, the present consensus was formulated. This consensus addresses 12 clinical questions covering syndrome types, preventive care, integrated prevention and treatment strategies, and non-pharmacological therapies for RH. It highlights the characteristics of being 'guided by the holistic thinking of TCM, centered on syndrome differentiation and treatment, and supported by precise Western medical interventions', thereby establishing an integrated diagnosis and treatment strategy tailored to the Chinese RH population. This consensus is expected to promote innovation in the standardized integrated management of RH in China, improve the overall level of RH prevention and treatment, and provide significant clinical and social value.  
      关键词:resistant hypertension;integrated traditional Chinese and western medicine;expert consensus   
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    • CHEN Yuanyuan, GUO Ye, CHANG Zangwei, QI Dahe, KONG Lingbo
      Vol. 32, Issue 15, Pages: 181-192(2026) DOI: 10.13422/j.cnki.syfjx.20261326
      摘要:ObjectiveTo investigate the effects of Naoxin'an Capsules (NXA) as an adjunct to conventional Western medicine on neurological function, functional independence, activities of daily living (ADL), and traditional Chinese medicine (TCM) syndrome elements in patients with acute cerebral infarction (ACI) due to Qi deficiency and blood stasis based on real-world data.MethodsA prospective cohort study based on a registry was conducted. A total of 470 hospitalized patients with ACI due to Qi deficiency and blood stasis treated in multiple centers between September 2023 and May 2025 were enrolled. According to their actual treatment regimens, the patients were assigned into three groups: the treatment group (n=126, receiving conventional Western medicine plus NXA), the Chinese patent medicine control group (n=154, receiving conventional Western medicine plus other stroke-related Chinese patent medicines, serving as a representative of heterogeneous mixed Chinese patent medicine regimens commonly used in clinical practice), and the Western medicine control group (n=190, receiving conventional Western medicine alone). All the patients were followed up for 3 months. The primary outcome measure was the change in the National Institutes of Health Stroke Scale (NIHSS) score on day 14 after stroke onset. Secondary outcome measures included longitudinal changes in the rate of functional independence [modified Rankin scale (mRS)≤2] and the rate of favorable ADL performance [(Barthel Index (BI)≥90] from baseline to day 14 and 3 months after stroke onset, as well as changes in TCM syndrome element scores from baseline to day 14 after stroke onset. Adverse events occurring within 3 months were also recorded.ResultsThe baseline confounders were adjusted. (1) Neurological function: Compared with the pre-treatment (baseline) value, the NIHSS scores on day 14 after stroke onset decreased in all the three groups (all adjusted P<0.01). On day 14 after stroke onset, compared with the Western medicine control group, both the treatment group and the Chinese patent medicine control group exhibited greater reductions in NIHSS score (change values) (both adjusted P<0.05), while no significant difference was observed between the treatment group and the Chinese patent medicine control group. (2) Functional prognosis: Longitudinal analysis based on generalized estimating equations (GEE) revealed that the rates of functional independence and favorable ADL performance increased over time across all the groups (time main effect, both adjusted P<0.01), with significant intergroup differences in improvement trends (interaction effect, both adjusted P<0.01). Compared with pre-treatment values, both rates increased on day 14 and 3 months after stroke onset in all the groups (all adjusted P<0.05). On day 14 after stroke onset, the two rates were higher in the treatment group than in the Western medicine control group (both adjusted P<0.05). The treatment group demonstrated superior outcomes compared with both control groups (all adjusted P<0.05) 3 months after stroke onset. (3) TCM syndrome elements: Compared with pre-treatment values, the scores of internal wind, phlegm-dampness, blood stasis, and Qi deficiency decreased on day 14 after stroke onset in all the three groups (all adjusted P<0.01), whereas only the treatment group showed a reduction in internal fire score (adjusted P<0.05). Both Chinese medicine groups exhibited lower phlegm-dampness scores than the Western medicine control group (both adjusted P<0.05). Furthermore, the treatment group showed greater reductions in blood stasis and Qi deficiency scores than the two control groups (both adjusted P<0.05). (4) Safety analysis: No significant difference was observed in the incidence of adverse events between the treatment group and the control groups.ConclusionEarly use of NXA as an adjunct to conventional Western medical therapy is associated with favorable prognostic outcomes in ACI patients with the syndrome of Qi deficiency and blood stasis. Its therapeutic effect exhibits a temporal pattern. On day 14 after stroke onset, NXA specifically alleviates the core TCM syndrome elements of Qi deficiency and blood stasis, and demonstrates superiority in improving neurological function and functional prognosis compared with conventional Western medicine alone. Three months after stroke onset, NXA outperforms both conventional Western medicine and the heterogeneous mixed regimens used in this study in terms of functional prognosis. Moreover, NXA maintains a favorable safety profile throughout the study period.  
      关键词:acute cerebral infarction;Naoxin'an Capsules (NXA);Qi deficiency and blood stasis;clinical efficacy;real-world study   
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    • BAI Jing, CHEN Liming, LI Taixian, LI Xiaoliang, DONG Shiyu, ZHAO Jiyang, XU Genrong, ZHAO Wanning, LI Dandan, GUO Shengjun, GONG Chunzhu, LIN Na, MI Baohong, CHEN Yuefeng, CHEN Weiheng
      Vol. 32, Issue 15, Pages: 193-201(2026) DOI: 10.13422/j.cnki.syfjx.20251838
      摘要:ObjectiveTo evaluate the clinical efficacy and safety of Osteoking in treating knee osteoarthritis (KOA) with the pattern of liver-kidney deficiency combined with blood stasis, providing evidence-based medical evidence for its clinical application.MethodsA multicenter, randomized, double-blind, double-dummy, positive-drug parallel-controlled design was adopted. A total of 252 KOA patients who met the inclusion criteria were enrolled from 17 Grade A tertiary hospitals across China between February 2024 and September 2024. These patients were randomly assigned at a 2∶1 ratio into the experimental group (168 cases) and the control group (84 cases). The experimental group was given Osteoking plus placebo of Gukang capsules, while the control group was given Gukang capsules plus placebo of Osteoking, with a 4-week treatment course. Baseline data of patients in the two groups were compared, including age, gender, height, weight, body temperature, resting heart rate, respiration, systolic blood pressure, diastolic blood pressure, allergy history, and history of comorbid diseases. The visual analog scale (VAS) score for knee pain was set as the primary efficacy indicator, while the secondary efficacy indicators included graded quantitative scores for major symptoms/signs and traditional Chinese medicine (TCM) syndromes, disappearance rate of individual major symptoms/signs/TCM syndromes, total Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) score, and WOMAC scores for pain, stiffness, and daily activities. Meanwhile, safety was evaluated, with assessments conducted once before treatment, and at 2 weeks and 4 weeks after treatment respectively. The differences in indicators before and after treatment were calculated at 2 weeks and 4 weeks post-treatment.ResultsBaseline data showed no statistically significant differences between the two groups before intervention (P<0.05), indicating comparable baseline characteristics of the enrolled subjects. After treatment, the Visual Analogue Scale (VAS) score was significantly lower in the experimental group than in the control group (P<0.05). The disappearance rates of traditional Chinese medicine (TCM) syndromes including joint pain, joint swelling and lassitude-fatigue were markedly higher in the experimental group (P<0.05). Additionally, the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain subscore decreased more prominently in the experimental group relative to the control group (P<0.05). No significant intergroup differences were observed in the incidence of adverse events and adverse drug reactions (P<0.05), and all 3 severe adverse events were assessed to be unrelated to the investigational drug.ConclusionOsteoking can significantly alleviate knee pain in patients with KOA presenting with the syndrome of liver-kidney deficiency complicated with blood stasis, improve local joint symptoms, and demonstrate a favorable safety profile. Its efficacy is superior to that of Gukang capsules. Therefore, this treatment is recommended for clinical application.  
      关键词:Osteoking;knee osteoarthritis;liver-kidney deficiency and blood stasis;randomized controlled trial;visual analog scale;western ontario and mcmaster universities osteoarthritis index (WOMAC)   
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    • LI Guangsen, FAN Maorong, WANG Bing, YUAN Shasha, SHI Xia, LIANG Yanxia, WANG Wenwen, LIU Fenggu
      Vol. 32, Issue 15, Pages: 202-209(2026) DOI: 10.13422/j.cnki.syfjx.20251222
      摘要:ObjectiveTo evaluate the efficacy and safety of Qingfei Litan Prescription in the treatment of stable bronchiectasis with airway mucus hypersecretion (syndrome of phlegm-heat accumulation in the lungs and deficiency of both spleen and kidney).MethodsA total of 68 patients with airway mucus hypersecretion in stable bronchiectasis were randomized into an observation group and a control group, with 34 patients in each group. The observation group was treated with Qingfei Litang Prescription granules, while the control group received a placebo of Qingfei Litang prescription. At the same time, both groups received basic treatment for a course of 3 months. The scores of the Cough and Sputum Assessment Questionnaire (CASA-Q), 24 h sputum volume, symptom grading and quantitative scores, levels of sputum mucin 5AC (MUC5AC) and neutrophil elastase (NE), lung function indicators, and inflammatory marker levels of the two groups were compared before and after treatment. The collected data were statistically analyzed in SPSS 25.0 software.ResultsAfter treatment, the observation group showed increases in the scores of four domains: cough symptom (COUS), cough influence (COUI), sputum symptom (SPUS), and sputum influence (SPUI) (P<0.05), and the control group showed increases in the scores of three domains: COUS, COUI, and SPUS (P<0.05) and an insignificant increase in the score of SPUI domain. After treatment, the 24 h sputum volume decreased in both groups (P<0.05) and the decrease was larger in the observation group than in the control group (P<0.05). The quantitative total score of symptom grading and the score of airway mucus hypersecretion symptoms decreased in both groups (P<0.05), and the observation group showed larger decreases than the control group (P<0.05). The sputum MUC5AC level decreased in both groups (P<0.05). The NE level decreased in the observation group (P<0.05), while the decrease in the control group was not significant. The lung function improved after the treatment in both groups, with the improvement being significant in terms of FEV1/FVC ratio (P<0.05), and the improvement of the observation group was better than that of the control group (P<0.05). The erythrocyte sedimentation rate (ESR) of the observation group (P<0.05), while that of the control group decreased insignificantly. Neither group showed obvious adverse reactions or abnormality in safety indexes during the treatment period.ConclusionQingfei Litan prescription can significantly ameliorate the cough and expectoration and traditional Chinese medicine symptoms, significantly reduce the 24 h sputum volume, down-regulate the levels of MUC5AC and NE, and improve the lung function to a certain degree in the patients suffering from stable bronchiectasis with airway mucus hypersecretion (syndrome of phlegm-heat accumulation in the lungs and deficiency of both spleen and kidney), demonstrating good clinical application value.  
      关键词:Qingfei Litan prescription;clearing and tonifying method;airway mucus hypersecretion;bronchiectasis;clinical study   
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    • YU Ting, TANG Chunyan, SHANGGUAN Jianhui, YANG Ping, QU Xinhui
      Vol. 32, Issue 15, Pages: 210-216(2026) DOI: 10.13422/j.cnki.syfjx.20251228
      摘要:ObjectiveTo investigate the clinical efficacy of kidney-warming and spleen-strengthening therapy combined with conventional treatment in patients with Parkinson's disease (PD), as well as its effects on gut microbiota dysbiosis and cognitive function, providing a new approach for the integrated treatment of PD with traditional Chinese and Western medicine.MethodsNinety patients with PD admitted to Jiangxi Provincial People's Hospital from March 2023 to April 2024 were randomly divided into a control group (45 cases, treated with conventional Western medicine, Levodopa/Benserazide tablets) and a study group (45 cases, treated with Wenre Jianpi Formula in addition to conventional Levodopa/Benserazide tablets). The Unified Parkinson's Disease Rating Scale (UPDRS), Montreal Cognitive Assessment (MoCA), 39-item Parkinson's Disease Questionnaire (PDQ-39), and gut microbiota were evaluated and compared between groups.ResultsCompared with pretreatment values, patients in the study group showed significantly decreased UPDRS and PDQ-39 scores (P<0.05), significantly increased MoCA scores (P<0.05), and significantly increased levels of Lactobacillus and Bifidobacterium (P<0.05). After treatment, compared with the control group, the study group exhibited significantly lower UPDRS and PDQ-39 scores (P<0.05) and significantly higher MoCA scores (P<0.05). The overall clinical efficacy based on UPDRS, PDQ-39, and MoCA scores in the study group was significantly better than that in the control group (P<0.05).ConclusionKidney-warming and spleen-strengthening therapy combined with conventional treatment significantly improves UPDRS and MoCA scores and enhances quality of life in patients with PD. The increased abundance of Lactobacillus and Bifidobacterium in the gut microbiota may be associated with improvements in cognitive function, providing support for integrated traditional Chinese and Western medicine treatment.  
      关键词:traditional Chinese medicine kidney-warming and spleen-strengthening therapy;conventional treatment;Parkinson's disease;gut microbiota dysbiosis;cognitive function   
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    • YUAN Ci, JIANG Jiamin, QI Junsheng, XIAO Zhi'en, YI Ziyuan, YING Tianhao, LIU Ming, YIN Fuqiang
      Vol. 32, Issue 15, Pages: 217-224(2026) DOI: 10.13422/j.cnki.syfjx.20260513
      摘要:ObjectiveTo identify the pathogen species responsible of Epimedium leaf blight in Wanzhou, Chongqing, investigate its biological characteristics, and screen effective fungicides, thereby providing a theoretical basis for disease control in production.MethodsThe pathogen was isolated through the tissue isolation method. Pathogenicity was verified according to Koch's postulates. The pathogen was identified based on morphological observation and multi-gene phylogenetic analysis. The biological characterization of the pathogen and fungicide screening were conducted based on the mycelial growth rate method.ResultsThe pathogen formed circular colonies, with sparse gray-brown mycelia in the center and dense white mycelia at the edge. Multi-gene phylogenetic analysis showed that the pathogen clustered in the same clade as Diaporthe hongkongensis, with a support rate of 100%. This result, combined with morphological characteristics, identified the pathogen causing the leaf blight of Epimedium in Wanzhou District of Chongqing as D. hongkongensis. The mycelia grew the fastest in the corn meal agar, potato dextrose agar, and oatmeal agar with soluble starch as the carbon source and peptone as the nitrogen source at 28 ℃, light-dark alternation and total darkness, and pH 6.0. Among the six chemical fungicides, prochloraz 45% ME had the best inhibitory effect, with an median effective concentration(EC50) of 0.040 mg·L-1. Among the five biological fungicides, tetramycin 0.3% AS had the best inhibitory effect, with an EC50 of 0.819 mg·L-1.ConclusionThis study is the first to report that D. hongkongensis causes the leaf blight of Epimedium. Chemical fungicides such as 45% prochloraz and biological fungicides such as 0.3% tetramycin have strong inhibitory effects on D. hongkongensis.  
      关键词:Epimedium;Diaporthe;leaf blight;biological characteristics;fungicide screening   
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    • CHEN Ningmei, ZHAO Dan, YANG Changgui, XIAO Chenghong, SHI Haixia, HU Yiming, KANG Chuanzhi, ZHAN Zhilai
      Vol. 32, Issue 15, Pages: 225-237(2026) DOI: 10.13422/j.cnki.syfjx.20252062
      摘要:This paper systematically collated and textually investigated the historical evolution of the name, origin, scientific name revision, producing area, quality evaluation, harvesting, processing, properties, efficacy, and indications of Uncariae Ramulus cum Uncis by consulting the ancient materia medica, medical books, and prescription books, in combination with modern literature, aiming to provide a reference for the development and utilization of famous classical formulas containing Uncariae Ramulus cum Uncis. After herbal textual research, Uncariae Ramulus cum Uncis was first recorded in Mingyi Bielu, named "Diaoteng", and then the name of "Gouteng" was first appeared in Bencao Mengquan in the Ming dynasty. Subsequent herbals mostly adopted the name. And there were other nicknames such as Diaoteng, Diaogouteng, and Shuanggouteng. The mainstream origin of Uncariae Ramulus cum Uncis was Uncaria rhynchophylla or U. sinensis in ancient times. In modern times, there were five types of mainstream origins, including U. rhynchophylla, U. sinensis, U. macrophylla, U. hirsuta, and U. sessilifructus. Since the Southern and Northern dynasties, the producing areas recorded were mainly in provinces such as Shaanxi, Sichuan, Chongqing, Guizhou, Hunan, Hubei, and Jiangxi. In modern and contemporary periods, the producing area expanded to most of the southern part of China, and the medicinal materials with the best quality were produced in Zunyi of Guizhou province, Guilin of Guangxi Zhuang Autonomous Region, and Wenzhou of Zhejiang province. The medicinal parts of Uncariae Ramulus cum Uncis were the stem bark and hooks during the Tang and Song dynasties, became mainly hooks in the Ming and Qing dynasties, and are now mainly stems with hooks. Since the Ming dynasty, the best quality was considered tender. In modern and contemporary periods, the best quality is considered to have double hooks, tender texture, and purple-red color. The ancient harvest time of Uncariae Ramulus cum Uncis was March of the lunar calendar, while in modern time, the harvest occurs in autumn and winter. In ancient times, Uncariae Ramulus cum Uncis was chiefly processed by cutting. However, in modern times, it is cut into sections and then either steamed before drying or sun-dried directly. In ancient times, Uncariae Ramulus cum Uncis was thought to have a slightly sweet taste with a slightly cold property. In modern times, the expression of property and flavour is not unified. Its channel tropism was attributed to the Jueyin meridians of both hand and foot as well as all twelve regular meridians in the Ming dynasty. Its meridian tropism shifted to the hand and foot Jueyin meridians as well as the heart and liver meridians in the Qing dynasty. Modern pharmacopoeia records attribute it to the liver and pericardium meridians. The efficacy of Uncariae Ramulus cum Uncis is basically consistent in ancient and modern records, mainly used for convulsive seizures, pediatric crying, headaches, dizziness, and so on. Based on the research results, it is suggested that U. rhynchophylla or U. sinensis can be used as the medicinal origin for the development of famous classical formulas containing Uncariae Ramulus cum Uncis. The processing method can be determined according to the requirements of formulas. If the processing requirements are not specified, it may be cut into segments and used medicinally after either direct sun-drying or steaming followed by sun-drying.  
      关键词:Uncariae Ramulus Cum Uncis;herbal textual research;scientific name;origin;producing area;quality evaluation;harvesting and processing   
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    • YE Du, YU Yunfeng, SU Siya, WANG Ying, YIN Yuman, CHU Shuzhou, ZHU Junping, YU Rong
      Vol. 32, Issue 15, Pages: 238-244(2026) DOI: 10.13422/j.cnki.syfjx.20260892
      摘要:Diabetic ulcer (DU), a severe chronic complication of diabetes, is characterized by delayed healing and high recurrence rates, significantly impairing patients' quality of life and imposing a substantial socioeconomic burden. Based on the traditional Chinese medicine (TCM) theory of "Gaozhuo" and combined with the modern medical concept of the "skin-gut axis", this study systematically explored the evolutionary pathophysiology of DU and its intrinsic relationship with microecological imbalance, and proposed potential TCM intervention strategies. According to TCM principles, spleen dysfunction in transportation led to the abnormal metabolism of nutrients, resulting in the pathological formation of Gaozhuo. Gaozhuo accumulated internally, descended to the intestines, and disrupted the gut microbiota. Over time, Gaozhuo stagnated, transformed into heat, spread externally to the striated layer, and blocked collaterals, forming a "spleen-gut-skin" pathological chain that ultimately impaired skin barrier function and delayed wound healing. Modern research demonstrated significant dysbiosis in both gut and skin microbiota in DU patients, with systemic inflammation and immune dysregulation identified as key contributors to the refractory nature of DU. TCM compounds and their active components can modulate the gut microbiota structure, enhance intestinal barrier integrity, and suppress inflammatory responses through multi-target and multi-pathway mechanisms. These effects further improved the skin microenvironment and promote ulcer healing via the skin-gut axis. Such intervention strategies aligned closely with the TCM therapeutic approach of "invigorating spleen, resolving turbidity, removing stasis, and unblocking collaterals", highlighting the holistic regulatory advantage of treating from the perspective of the spleen-stomach system while targeting the microbiota. By integrating the theory of Gaozhuo with the skin-gut axis mechanism, this study constructed a theoretical framework combining Chinese and western medicine for DU prevention and treatment, offering novel perspectives and directions for clinical practice and future research.  
      关键词:theory of "Gaozhuo";skin-gut axis;diabetic ulcer;gut microbiota   
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    • YANG Fan, ZHANG Yan, YUAN Ziyang, YANG Guo, MU Qirui, ZHOU Chuqing, ZHAO Yilin, GAO Cui, WANG Yifei
      Vol. 32, Issue 15, Pages: 245-255(2026) DOI: 10.13422/j.cnki.syfjx.20261295
      摘要:Chronic heart failure (CHF) is the end result of various cardiovascular diseases,with high morbidity and mortality,which has been widely concerned by the public. Recent studies have shown that ventricular remodeling is an important physiological and pathological mechanism of heart failure. Therefore,targeted regulation of ventricular remodeling is of great significance for the prevention and treatment of chronic heart failure. The theory of host-guest interaction and the theory of collateral disease are both important parts of the theoretical system of traditional Chinese medicine. The combination of the two can enrich the system of syndrome differentiation and treatment of diseases in traditional Chinese medicine. The theory of host-guest interaction was first seen in the theory of epidemic febrile disease written by Wu Youke,a doctor in the Ming dynasty,and is now used to guide the treatment of various chronic diseases. In the pathogenesis of ventricular remodeling in chronic heart failure,the pathogenesis characteristics of deficiency in origin and excess in superficiality,deficiency and excess are highly consistent with the connotation of "host-guest interaction" deficiency and pathogen accumulation,and collaterals dystrophy. The theory of collateral disease takes collaterals as the core,emphasizing that "collaterals are smooth and the viscera are peaceful". This disease also belongs to the category of "collateral disease". Therefore,based on the theory of "host-guest interaction-collateral disease",this paper holds that the deficiency of heart Qi and the dystrophy of collaterals are the root of the disease. The treatment should supplement the heart qi and nourish the collaterals to consolidate its root, phlegm and blood stasis,collaterals urgent as the key to the disease,the treatment of blood stasis phlegm,dredging collaterals,in order to slow its potential, turbidity and toxin are endogenous,and the accumulation of collaterals is the pathogenesis. The treatment needs to detoxify and dredge collaterals,eliminate accumulation and disperse knots,so as to save the danger. Based on the theory of "host-guest interaction-collateral disease",this paper discusses the pathogenesis evolution of "deficiency-stasis-phlegm-toxin-accumulation" of ventricular remodeling in chronic heart failure,in order to broaden the cognition of traditional Chinese medicine on ventricular remodeling in chronic heart failure,and provide theoretical basis and treatment ideas for delaying ventricular remodeling and improving chronic heart failure.  
      关键词:chronic heart failure;"host-guest interaction-collateral disease" theory;ventricular remodeling;traditional Chinese medicine;mechanism of action   
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    • Pharmacological Effect and Microscopic Mechanisms of Shenling Baizhu San AI导读

      LIAN Kun, JIANG Yang, WANG Xueqin, MENG Lichong, LI Lin, HU Zhixi
      Vol. 32, Issue 15, Pages: 256-265(2026) DOI: 10.13422/j.cnki.syfjx.20251515
      摘要:Shenling Baizhu San is a classic prescription recorded in Taiping Huimin Heji Jufang, mainly used for treating spleen deficiency and excessive dampness syndrome. The core principle of formula is invigorating the spleen and replenishing Qi to restore ascending and descending of Qi movement, and eliminating dampness and regulating the middle to smooth the flow of Qi. It has the characteristics of being warm but not dry and nourishing but not harsh. This article systematically analyzes the formulation characteristics, material basis, pharmacological effects and mechanisms of Shenling Baizhu San. Shenling Baizhu San has multiple pharmacological effects, including anti-inflammation, anti-oxidative stress, improvement of immune function, repair of intestinal mucosa, regulation of gut microbiota homeostasis, and regulation of cell apoptosis and autophagy. These mechanisms of action are highly consistent with modern medicine's understanding of the pathophysiology of various diseases, providing theoretical support for its application in the treatment of multiple diseases. However, its complex composition and mechanisms of action still make it difficult to deeply analyze its specific action pathways and targets. Future research needs to further integrate modern science and technology, such as metabolomics, proteomics and genomics, to more comprehensively reveal its mechanisms of action. In addition, clinical trials shall be carried to verify its efficacy and safety in the treatment of different diseases, thereby providing stronger evidence to support its clinical application.  
      关键词:Shenling Baizhu San;pharmacological effects;mechanism of action;gutmicroecology;inflammatory response   
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    • HU Yang, HU Suqin, ZENG Shuo, LUO Lei, LI Mingyan, ZHANG Qinsheng
      Vol. 32, Issue 15, Pages: 266-274(2026) DOI: 10.13422/j.cnki.syfjx.20251229
      摘要:Gastric cancer, as a highly lethal malignant tumor in the digestive system, is particularly severe in China. At present, Western medicine treatment has shown some effectiveness in inhibiting tumor growth, alleviating patient symptoms, and delaying disease progression. However, there are still significant side effects, sustained increase in drug resistance, and limited improvement in patient survival rates, which make it difficult for the overall effectiveness of gastric cancer treatment to be satisfactory. Therefore, seeking more efficient and safe treatment strategies has become a key issue that urgently needs to be addressed in the field of oncology. The adenosine monophosphate-activated protein kinase (AMPK) signaling pathway plays a key regulatory role in the pathological processes of gastric cancer cell proliferation, differentiation, apoptosis, and autophagy, and is an important target for gastric cancer treatment research. Traditional Chinese medicine has shown unique advantages in the treatment of gastric cancer. Through multiple pathways, mechanisms, and synergistic effects, it can effectively prevent postoperative recurrence and metastasis, significantly reduce adverse reactions of radiotherapy and chemotherapy, and improve patients' quality of life. It has become a key component of the comprehensive treatment system for gastric cancer. Numerous research results have shown that active ingredients in traditional Chinese medicine, such as alkaloids, terpenes, flavonoids, polyphenols, isothiocyanates, and polysaccharides, as well as classic traditional Chinese medicine compounds such as Jinguoweikang capsules, Weining granules, Babaodan, and Zuojin pills, exhibit significant regulatory effects on AMPK and its interaction signaling pathways. This is mainly achieved through mechanisms such as inducing autophagy and apoptosis in gastric cancer cells, inhibiting epithelial-mesenchymal transition, reversing drug resistance, inhibiting lipid metabolism, and arresting the cell cycle, thereby effectively inhibiting gastric cancer. This article comprehensively reviewed and summarized the relevant research on the anti-gastric cancer effects of traditional Chinese medicine in recent years, focusing on the mechanism of traditional Chinese medicine regulating the AMPK signaling pathway in the treatment of gastric cancer. The aim is to provide new ideas and reference for the development of new anti-gastric cancer drugs in clinical practice.  
      关键词:adenosine monophosphate-activated protein kinase (AMPK);signaling pathway;traditional Chinese medicine;gastric cancer   
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    • ZENG Zhaolu, GUO An, SUN Luyan, HE Tiantian, SUN Yuefeng, LIU Shijia, FAN Lanxin, FENG Jihong, SUN Zengtao
      Vol. 32, Issue 15, Pages: 275-286(2026) DOI: 10.13422/j.cnki.syfjx.20260465
      摘要:The mortality rate of severe pneumonia (SP) remains persistently high, with the core challenge lying in the dynamic evolution and precise regulation of immune imbalance. This paper systematically reviewed the core characteristics and pathological mechanisms of the five stages of SP, including immune overactivation, immune tolerance, immunosuppression, immune exhaustion, and immunoparalysis. It further elaborated on the progress of immune quantification assessment systems and their guiding value for individualized treatment, from both traditional indicators and emerging evaluation techniques. On this basis, the paper deeply integrated the pathogenesis evolution patterns of traditional Chinese medicine theory which is the "struggle between healthy Qi and pathogenic factors and the transformation between deficiency and excess". Different immune phenotypes were logically correlated with pathogenetic stages of traditional Chinese medicine. The paper systematically demonstrated the molecular mechanisms by which traditional Chinese medicine monomers (e.g., baicalin, artesunate, and schisandrin B) exert targeted regulatory effects through regulating signaling pathways such as Toll-like receptor (TLR)/nuclear factor-κB (NF-κB), NOD-like receptor family pyrin domain-containing 3 (NLRP3), nuclear factor erythroid 2-related factor 2 (Nrf2)/peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), and silent information regulator 1 (SIRT1)/adenosine monophosphate-activated protein kinase (AMPK). It also highlighted how traditional Chinese medicine formulas (e.g., Maxing Shigan Tang, Lianhua Qingke tablets, and Shenfu injection) achieve a holistic regulatory advantage of the dynamic balance of "eliminating pathogenic factors" (anti-inflammation) and "strengthening healthy Qi" (immune reconstitution) by the synergistic action of multiple components on multiple targets and pathways across different immune stages. By integrating the pathogenesis evolution of traditional Chinese medicine with modern immune quantification assessment, this approach facilitates the construction of an immunophenotype-guided integrated traditional Chinese and Western medicine treatment strategy, enabling stepwise and individualized interventions. This provides a theoretical basis and practical direction for breaking through the shallow integration mode of corresponding terms between Chinese and Western medicine and achieving precision immunotherapy for SP.  
      关键词:severe pneumonia;immune imbalance;traditional Chinese medicine;strengthening healthy Qi and eliminating pathogenic factor;immune assessment   
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    • LYU Peiyao, MENG Binru, LIU Chuanfeng, LI Jiaxin, LI Bin
      Vol. 32, Issue 15, Pages: 287-296(2026) DOI: 10.13422/j.cnki.syfjx.20260365
      摘要:Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disorder of insidious onset, with major clinical characteristics of cognitive decline and a gradual loss of the ability to perform activities of daily living. Mitochondria, as central regulators of energy metabolism, are essential for maintaining the normal vitality and physiological functions of brain neurons. Mitochondrial dynamics homeostasis is the core link to maintaining the normal function of mitochondria, including mitochondrial fission, fusion, transport, autophagy, and other biological processes. The imbalance in this process can form a vicious circle, leading to the abnormal deposition of β-amyloid (Aβ) and hyperphosphorylation of the Tau protein. It can also aggravate the pathological progression of AD by inducing synaptic function damage and accelerating neuronal apoptosis. In recent years, traditional Chinese medicine has provided potential new ideas and effective solutions for the prevention and treatment of AD with its unique advantages of multiple components and multiple dimensions. This paper thoroughly investigated the critical regulatory targets and the signaling pathway mechanisms of traditional Chinese medicine in maintaining mitochondrial dynamics homeostasis. It systematically reviewed the potential molecular mechanisms and latest research progress of traditional Chinese medicine in treatment of AD by targeting mitochondrial dynamics imbalance. The findings aim to serve as a reference and foundation for clinical treatments and drug research and development of AD.  
      关键词:Alzheimer's disease;mitochondrial dynamics;mechanism of action;traditional Chinese medicine;research progress   
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    • ZHAO Fangfang, GUO Yanke, WANG Xueke, PANG Botong, ZHU Yanqiang, QIN Yang, CUI Yinglin
      Vol. 32, Issue 15, Pages: 297-308(2026) DOI: 10.13422/j.cnki.syfjx.20252238
      摘要:Neurodegenerative diseases are a major disease caused by progressive degeneration of neurons and loss of brain tissue. As high-energy-consuming cells, neurons are highly dependent on the energy supply and homeostasis maintenance of mitochondria for their survival and function. Mitochondrial dysfunction not only triggers an energy crisis, but also leads to oxidative stress imbalance and activation of cell apoptosis, which is a key mechanism in the onset and progression of neurodegenerative diseases. Therefore, maintaining mitochondrial quality control is of great significance in the prevention and treatment of neurodegenerative diseases, among which mitochondrial autophagy, as the core mechanism for selectively clearing damaged mitochondria, has become a hotspot of current research. The PTEN-induced putative kinase 1 (PINK1)/Parkin RBR E3 ubiquitin-protein ligase (Parkin) pathway is the most classic and critical signaling pathway in mitochondrial autophagy, playing a central role in mediating mitochondrial clearance and maintaining neuronal survival. In recent years, although the molecular mechanism of the PINK1/Parkin pathway has been widely studied, there is still a lack of systematic reviews on how traditional Chinese medicine (TCM) regulates this pathway to treat neurodegenerative diseases. Based on this research gap, this article focuses for the first time on the mechanism of TCM monomers and formulas regulating mitochondrial autophagy through the PINK1/Parkin pathway. It systematically reviews their neuroprotective effects in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease, and deeply explores their multi-component, multi-target, and overall regulatory advantages. In addition, this article also combines the theories of "syndrome differentiation and treatment" and "holistic view" of TCM to analyze the common laws and individual characteristics of TCM regulation of this pathway, and proposes strategies for future in-depth research using cutting-edge technologies such as chemical proteomics and disease syndrome combined organoid models. The aim is to provide a new perspective for explaining the modern mechanism of TCM in the prevention and treatment of neurodegenerative diseases, and to provide a theoretical basis and ideas for the development of multi-target, low-toxicity neuroprotective drugs.  
      关键词:neurodegenerative diseases;traditional Chinese medicine (TCM);TCM formulas;PTEN-induced putative kinase 1 (PINK1)/Parkin RBR E3 ubiquitin-protein ligase (Parkin);progress   
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    • LIU Wei, CHEN Rongchang
      Vol. 32, Issue 15, Pages: 309-316(2026) DOI: 10.13422/j.cnki.syfjx.20252507
      摘要:Cardiovascular diseases represent a leading cause of death worldwide. Heart failure (HF), as the end stage of a range of cardiovascular conditions, is characterized by high incidence and mortality rates, posing a major challenge to global public health. As the population aging in China is aggravating, the incidence of HF keeps rising, which underscores the importance of in-depth research into its pathogenesis and the discovery of drugs targeting novel mechanisms. The pathogenesis of HF is complex, involving multiple interrelated processes such as aberrant energy metabolism, mitochondrial dysfunction, myocardial injury, and overactivation of the neuroendocrine system, which collectively drive the onset and progression of HF. In the pursuit of multi-target intervention strategies, traditional Chinese medicine (TCM) demonstrates unique advantages. Ginseng Radix et Rhizoma, a highly valuable herbal medicine, is known for its abilities to greatly tonify primordial Qi, restore pulse, and secure collapse. Ginsenosides, the primary bioactive constituents of Ginseng Radix et Rhizoma, exhibit remarkable cardiovascular protective effects. In recent years, there has been increasing research on the protective effects and mechanisms of Ginseng Radix et Rhizoma against HF. This article reviews the pathogenesis and key signaling pathways in HF, and elaborates on the protective effects and critical targets of well-characterized ginsenosides. The aim is to provide insights for further elucidating the pathogenesis of HF and the cardioprotective roles of ginsenosides, thereby facilitating the therapeutic exploitation of these compounds.  
      关键词:heart failure (HF);ginsenoside;mechanism of action;key target   
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    • MA Mengmeng, GUAN Xutao, SUN Shiling
      Vol. 32, Issue 15, Pages: 317-329(2026) DOI: 10.13422/j.cnki.syfjx.20252195
      摘要:The formula, Liuwei Dihuangwan (LWDH), first recorded in Key to Therapeutics of Children's Diseases (Xiao Er Yao Zheng Zhi Jue), is composed of six herbal medicines: Rehmanniae Radix Praeparata, Corni Fructus, Dioscoreae Rhizoma, Alismatis Rhizoma, Moutan Cortex, and Poria. It is one of the classic formulas for nourishing yin and tonifying the kidney. It has been included in the 2020 edition of the Pharmacopoeia of the People's Republic of China. The manufacturing process employs strictly selected high-quality medicinal materials and is optimized using modern pharmaceutical technologies, thereby effectively preserving the active constituents of the formula. The formula mainly contain organic acids, terpenoids, flavonoids, glycosides, and other compounds. Modern studies have demonstrated that LWDH possess a variety of pharmacological activities, including renal protection, antioxidant, antitumor, immunomodulatory, and lipid metabolism-regulating effects, and are widely used in the treatment of renal diseases, metabolic diseases, gynecological diseases, orthopedic diseases, neoplastic diseases, and pediatric diseases. This review summarizes the research progress on LWDH with respect to chemical constituents, pharmacological effects, and modern clinical applications. Furthermore, based on the concept of quality markers (Q-Markers), the potential Q-Markers of LWDH were predicted. Rehmannioside D, verbascoside, alisol B 23-acetate, alisol C 23-acetate, paeonol, pachymic acid, allantoin, loganin, and morroniside were identified as potential Q-Markers of the formula, providing a scientific basis for subsequent studies on this compound prescription and its quality control.  
      关键词:Liuwei Dihuangwan;quality markers;research progress;rehmannioside D;verbascoside   
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    • DU Qinyuan, QIN Congcong, LI Guochen, BA Tejin, ZHANG Shuanglin, BAO Bagenna, BAO Meiyu, KONG Li
      Vol. 32, Issue 15, Pages: 330-338(2026) DOI: 10.13422/j.cnki.syfjx.20252307
      摘要:Banxia Xiexintang (BXXXT) first recorded in the Treatise on Cold Damage (Shang Han Lun) and Synopsis of the Golden Chamber (Jin Gui Yao Lue) follows the principle of pungent dispersing and bitter descending, harmonizing the middle and descending adverse Qi, and reconciling both cold and heat. It is indicated for epigastric stuffiness, vomiting, and borborygmi caused by middle Yang impairment due to wrong application of the purgative method. According to the theory of treating different diseases with the same method, BXXXT targets the shared mechanism of epigastric stuffiness, vomiting, and borborygmi and has been applied in the treatment of multiple diseases in the upper energizer (gastroesophageal reflux and chemotherapy-induced mucositis), middle energizer (functional dyspepsia, chronic/atrophic gastritis, Helicobacter pylori-associated disease, and cross symptoms of spleen/stomach-liver/gallbladder), and lower energizer (ulcerative colitis and chemotherapy-related diarrhea). BXXXT demonstrates positive signals in terms of symptoms, endoscopy/pathology, eradication rates, and safety. From the perspective of mechanism, it suppresses Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB, mitogen-activated protein kinase (MAPK), and NOD-like receptor protein 3 (NLRP3), activates Kelch-like ECH-associated protein 1 (Keap1)/nuclear erythroid 2-related factor 2 (Nrf2) and PTEN-induced kinase 1 (PINK1)/Parkin, and restores tight junctions by up-regulating the expression of Zonula occludens-1 (ZO-1)/Occludin and inhibiting myosin light chain kinase (MLCK). BXXXT preserves interstitial cell of Cajal (ICC)-c-Kit and Ras-homolog gene family, member A (RhoA)/Rho-associated coiled-coil containing kinase (ROCK) while reducing transient receptor potential vanilloid 1 (TRPV1)/5-hydroxytryptamine (5-HT) sensitization. It remodels short-chain fatty acid (SCFA)-associated pathways of microbiota, rebalances farnesoid X receptor (FXR)/Takeda G protein-coupled receptor 5 (TGR5)-glucagon-like peptide-1 (GLP-1)/fibroblast growth factor 19 (FGF19), and engages vagal α7-neuronal nicotinic acetylcholine receptor (α7nAChR) to modulate gut-brain interaction. Translational anchors [diamine oxidase (DAO), D-lactate, bile-acid profiles/FGF19/GLP-1, helper T cells (Th17)/regulatory T cells (Treg), motilin (MTL), heart rate variability (HRV), and patient-reported outcomes (PROs)] support a coherent "pattern-biomarker-organ function-endpoint" chain, highlighting integrated anti-inflammatory, antioxidative, barrier-protective, pro-motility, microbiota-modulating, and metabolic effects.  
      关键词:Banxia Xiexintang;treating different diseases with the same method;mucosal barrier;gut microbiota;farnesoid X receptor (FXR)/Takeda G protein-coupled receptor 5 (TGR5) pathway   
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    • ZHONG Xinyu, GUO Jiangfan, LI Qingsong, LIU Tonghua, QIN Lingling, WU Lili, WANG Tingting
      Vol. 32, Issue 15, Pages: 339-346(2026) DOI: 10.13422/j.cnki.syfjx.20251824
      摘要:Diabetic peripheral neuropathy (DPN), as one of the most common chronic complications of diabetes mellitus, has a core pathologic mechanism closely related to ferroptosis in Schwann cells (SCs) induced by high glucose (HG) environment. Ferroptosis, iron-dependent lipid-peroxidation-driven programmed cell death, leads to SCs dysfunction through iron overload, lipid peroxidation, and dysregulation of the antioxidant system, which thereby causes peripheral nerve injury. In recent years, it has been found that bioactive monomers in traditional Chinese medicine can intervene in DPN through multi-targeted modulation of key pathways of ferroptosis. In regulating iron metabolism homeostasis, saponin constituents such as astragaloside Ⅳ and notoginsenoside R1 reduce intracellular free Fe2+ accumulation by down-regulating ferroportin 1 (FPN1). Flavonoids such as puerarin and quercetin activate FPN1 to promote iron exocytosis. Polyphenolic compounds, such as resveratrol and salvianolic acid A, maintain iron metabolism homeostasis through the hypoxia-inducible factor 2-alpha (HIF-2α), iron homeostasis, and other pathways, which reduce the increase in reactive oxygen species (ROS) triggered by the Fenton reaction. At the level of inhibition of lipid peroxidation, bioactive monomers target the activation of the antioxidant defense system. Paeoniflorin and quercetin promote glutathione (GSH) synthesis and enhance glutathione peroxidase 4 (GPX4) activity by up-regulating the expression of solute carrier family 7 member 11 (SLC7A11), effectively scavenging lipid peroxides. Astragaloside Ⅳ and magnolol promote the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2), induce the expression of antioxidant enzymes, such as heme oxygenase-1 (HO-1) and superoxide dismutase (SOD), and significantly reduce the levels of lipid peroxidation products, such as malondialdehyde (MDA). In addition, bioactive monomers in traditional Chinese medicine exert synergistic effects by modulating key signaling networks. Astragaloside Ⅳ inhibits p53-mediated ferroptosis sensitivity via the silent information regulator 1 (SIRT1)/p53 axis. Lycium barbarum polysaccharides and gastrodin repair mitochondrial function and block the release of mitochondrial ROS associated with ferroptosis. Naringenin and resveratrol reduce the expression of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and other inflammatory factors by inhibiting the nuclear factor- kappa B (NF-κB) pathway, indirectly alleviating oxidative stress injury. Bioactive monomers in traditional Chinese medicine of saponins, flavonoids, polyphenols, and polysaccharides inhibit ferroptosis in SCs through three major pathways: regulation of iron metabolism, enhancement of antioxidant capacity, and repair of cellular damage, which provides a new strategy for DPN treatment. Further clinical translational studies are needed to deepen the exploration of bioactive monomers of traditional Chinese medicine in the future.  
      关键词:ferroptosis;diabetic peripheral neuropathy;Schwann cells;bioactive monomers in traditional Chinese medicine;research progress   
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