最新刊期

    GUO Li, CHEN Hengwen, ZHAN Cun, YING Zhenzhen, WU Zuomin, JIN Shaoju, CAO Shangmei, HUANG Shengming, WANG Jin, YU Xiaotao

    DOI:10.13422/j.cnki.syfjx.20251329
    摘要:ObjectiveTo investigate the effects of modified Buyang Huanwu Tang on cerebral ischemia-reperfusion injury (CI/RI) in mice via the PTEN-induced putative kinase 1/E3 ubiquitin ligase (PINK1/Parkin) signaling pathway-mediated mitophagy, and to explore the underlying mechanism by which modified Buyang Huanwu Tang improves CI/RI.MethodsSeventy-two male C57BL/6J mice were randomly divided into six groups (n = 12 per group): Sham-operated group, middle cerebral artery occlusion/reperfusion (MCAO/R) model group, low-, medium-, and high-dose modified Buyang Huanwu Tang groups (8.84, 17.68, and 35.36 g·kg-1·d-1), and an aspirin group (13.00 mg·kg-1·d-1). Neurological deficit scores were assessed using the Zea-Longa method. Cerebral infarct volume ratio was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Histopathological changes and neuronal injury in brain tissues were observed using hematoxylin-eosin (HE) staining and Nissl staining. Apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. Mitochondrial ultrastructure in brain tissue was observed by transmission electron microscopy (TEM). Serum levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined by enzyme-linked immunosorbent assay (ELISA). The mRNA and protein expression levels of PINK1, Parkin, microtubule-associated protein light chain 3 (LC3B, LC3Ⅱ/Ⅰ), and p62 in brain tissues were detected by real-time quantitative reverse transcription PCR (Real-time PCR) and Western blot, respectively.ResultsCompared with the sham-operated group, the MCAO/R model group showed significantly increased neurological deficit scores and cerebral infarct volume ratios (P<0.01). Severe cortical injury on the infarct side was observed, characterized by decreased neuronal density, cytoplasmic vacuolation, nuclear pyknosis, a marked reduction in Nissl bodies, dissolution of Nissl bodies in the cytoplasm of some pyramidal neurons, and blurred cellular boundaries. The number of TUNEL-positive cells increased significantly (P<0.01). Mitochondria exhibited cristae membrane rupture and matrix vacuolation, with rupture of the outer mitochondrial membrane and formation of autophagosomes, the number of which increased significantly. Serum SOD activity decreased significantly (P<0.01), while MDA content increased significantly (P<0.01). In infarcted brain tissues of model mice, the relative mRNA expression and protein levels of PINK1, Parkin, and LC3B were significantly increased (P<0.05, P<0.01), whereas p62 mRNA and protein expression were significantly decreased (P<0.05, P<0.01), showing statistical significance. Compared with the model group, all treatment groups showed significantly decreased neurological deficit scores and cerebral infarct volume ratios (P<0.01). Neuronal density increased significantly, cytoplasmic vacuolation was alleviated, nuclear morphology tended to be more regular and clearer, Nissl body density increased significantly with reduced dissolution and improved contour clarity. The mitochondrial cristae structure was partially restored, with some mitochondria showing autophagosome encapsulation, and the degree of mitochondrial damage was alleviated. Serum SOD activity increased significantly (P<0.01), while MDA content decreased significantly. The mRNA and protein expression levels of PINK1, Parkin, and LC3Ⅱ/Ⅰ were significantly increased (P<0.05, P<0.01), while p62 mRNA and protein expression in the low- and medium-dose modified Buyang Huanwu Tang groups were significantly decreased (P<0.05, P<0.01), showing statistical significance.ConclusionModified Buyang Huanwu Tang can upregulate the protein expression levels of PINK1, Parkin, and LC3Ⅱ/Ⅰ and downregulate p62 protein expression, suggesting that it may improve CI/RI by regulating the expression of proteins related to the PINK1/Parkin signaling pathway. Regulation of the mitophagy pathway may be one of the mechanisms by which modified Buyang Huanwu Tang alleviates CI/RI in mice.  
    关键词:modified Buyang Huanwu Tang;Guiqi Tongmai mixture;cerebral ischemia-reperfusion injury;autophagy;PINK1/Parkin signaling pathway   
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    更新时间:2026-04-21

    HU Yang, HU Suqin, ZENG Shuo, LUO Lei, LI Mingyan, ZHANG Qinsheng

    DOI:10.13422/j.cnki.syfjx.20251528
    摘要:Liver cancer, as a malignant tumor with high incidence and mortality worldwide, has shown a year-by-year increase in both incidence and mortality in China. Currently, Western medicine has achieved certain efficacy in the clinical management of liver cancer in terms of inhibiting tumor growth, alleviating patient symptoms, and delaying disease progression. However, its limitations cannot be ignored. Significant side effects, increasingly severe drug resistance, and limited improvement in patient survival collectively make the overall therapeutic outcomes fall short of ideal expectations. Therefore, exploring more effective and safer treatment strategies has become a critical issue that urgently needs to be addressed in the field of oncology. The adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway plays a central regulatory role in the physiological processes of liver cancer cells, including proliferation, differentiation, apoptosis, and autophagy, and is considered a key molecular target for anti-liver cancer therapy. Traditional Chinese medicine (TCM), characterized by its multi-pathway and multi-mechanism synergistic effects, has become an important component of the current comprehensive treatment system for liver cancer. Among these, TCM monomeric compounds, owing to their well-defined chemical structures and precisely analyzable pharmacological mechanisms, represent an important breakthrough in anti-liver cancer drug development. Studies have shown that various TCM monomeric compounds, including flavonoids, alkaloids, polyphenols, saponins, terpenoids, and quinones, can regulate the AMPK/mTOR signaling pathway and its upstream and downstream protein expression. Through these mechanisms, they induce autophagy and apoptosis in liver cancer cells, inhibit aerobic glycolysis, reverse drug resistance, promote ferroptosis, block epithelial-mesenchymal transition, and inhibit angiogenesis, thereby effectively suppressing the growth and metastasis of liver cancer cells. Based on this, this article systematically reviews recent studies on TCM monomeric compounds in the treatment of liver cancer, and further analyzes in depth their mechanisms in regulating the AMPK/mTOR signaling pathway, so as to provide ideas and references for the development of new anti-liver cancer drugs.  
    关键词:adenosine monophosphate-activated protein kinase (AMPK);mammalian target of rapamycin (mTOR);monomer of traditional Chinese medicine;liver cancer;research progress   
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    更新时间:2026-04-21

    LIN Sitian, LIU Yuanjie, YIN Yi, LIU Shenlin, ZOU Xi

    DOI:10.13422/j.cnki.syfjx.20251924
    摘要:ObjectiveTo investigate the mechanisms by which Jianpi Yangzheng Xiaozheng prescription (JPYZXZ) treats poorly cohesive gastric carcinoma (PC-GC) through regulation of ubiquitin-specific peptidase 51 (USP51).MethodsIn vitro experiments: Cell viability and proliferation of PC-GC cell lines (MKN-45 and HGC-27) treated with different concentrations of JPYZXZ (2, 4, and 6 g·L-1) were assessed using Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell migration was evaluated by wound healing (scratch) and Transwell assays. The mRNA and protein expression levels of USP51, zinc finger E-box-binding homeobox 1 (ZEB1), and epithelial-mesenchymal transition (EMT)-related markers (e.g., E-cadherin) were detected by quantitative real-time PCR (qRT-PCR) and Western blot, respectively. Subsequently, stable MKN-45 and HGC-27 cell lines with USP51 knockdown (sh-USP51) and overexpression (oe-USP51) were constructed. Their migration ability and EMT-related protein expression were further evaluated by scratch assay, Transwell assay, and Western blot. In vivo experiments: A subcutaneous xenograft model of MKN-45 human gastric cancer was established in BALB/c nude mice. Thirty mice were randomly divided into six groups (NC, NC + JPYZXZ, sh-USP51, sh-USP51 + JPYZXZ, oe-USP51, and oe-USP51 + JPYZXZ), with five mice in each group. After successful modeling, mice in the treatment groups were administered JPYZXZ (30 g·kg-1) by gavage for 28 days. Body weight and tumor volume were monitored during the experiment. The expression levels of USP51 and EMT-related proteins in tumor tissues were detected by Western blot and immunohistochemistry (IHC).ResultsCompared with the blank group, the colony formation rate, wound healing rate, and number of migrated cells in MKN-45 and HGC-27 cells were significantly reduced in all JPYZXZ groups and the 5-fluorouracil (5-FU) group (P<0.05). The mRNA and protein expression levels of USP51 were decreased (P<0.05). The expression of ZEB1 and mesenchymal phenotype proteins (e.g., N-cadherin and vimentin) was reduced (P<0.05), whereas the expression of the epithelial marker E-cadherin was increased (P<0.05). Compared with the control group, USP51 expression was decreased in the sh-USP51 group and increased in the oe-USP51 group (P<0.05). Compared with the NC group, USP51 knockdown significantly reduced the migration and proliferation of gastric cancer cells (P<0.01), decreased the expression of ZEB1 and EMT-related proteins, and increased E-cadherin expression (P<0.05). In vivo results showed that JPYZXZ significantly inhibited the growth of xenograft tumors in nude mice (P<0.05) and markedly reversed the abnormal expression of EMT-related proteins in tumor tissues (P<0.05).ConclusionThe therapeutic mechanisms of JPYZXZ in PC-GC may be associated with inhibition of the EMT process via regulation of the USP51-ZEB1 signaling pathway.  
    关键词:Jianpi Yangzheng Xiaozheng prescription;poorly cohesive gastric carcinoma;ubiquitin-specific peptidase 51 (USP51);zinc finger E-box-binding homeobox 1 (ZEB1);epithelial-mesenchymal transition (EMT)   
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    更新时间:2026-04-14

    LI Siyu, DENG Shuangfei, DING Daiyue, SONG Changyue, SU Xiaohui, KONG Xiangying

    DOI:10.13422/j.cnki.syfjx.20260105
    摘要:ObjectiveTo study the marketed products and prescription characteristics of Chinese patent medicines for rheumatoid arthritis (RA) in China, thus providing support for clinical application and innovative research and development of Chinese patent medicines for RA.MethodsInformation on marketed Chinese patent medicines for RA treatment was collected. Preliminary data organization and statistical analysis were performed in Microsoft Excel 2021. Subsequently, the standardized prescriptions were analyzed via the Ancient and Modern Medical Case Cloud Platform (V2.3.9) across dimensions including medicinal properties, flavors, channel tropisms, usage characteristics, and formulation patterns.ResultsThis study ultimately included 311 marketed Chinese patent medicines for RA in China. Their initial market launch dates were mostly concentrated from the 1990s to the early 21st century. The National Basic Medical Insurance, Work-Related Injury Insurance, and Maternity Insurance Drug Directory included 89 Chinese patent medicines for RA. The primary dosage forms were tablets, capsules, medicated wines, and pills. After screening, 237 prescriptions were obtained, and the research on their origins was lagging. Among them, the Chinese patent medicines for treating wind-cold-dampness obstruction syndrome accounted for the highest proportion. The top three most frequently used medicinals were Angelicae Sinensis Radix, Notopterygii Rhizoma et Radix, and Saposhnikoviae Radix. Medicinal properties were primarily warm and plain, and flavors were mostly pungent, sweet, and bitter. The medicinals predominantly exhibited the liver and spleen channel tropism. Association rule analysis revealed that the herb pairs with the highest confidence were Chuanxiong-Angelicae Sinensis Radix and Myrrha-Olibanum. Cluster analysis yielded three medicinal combinations.ConclusionAlthough Chinese patent medicines for RA have application advantages, issues such as narrow syndrome coverage and insufficient innovation in dosage forms exist. Future development should focus on constructing an evidence-based system, strengthening the textual research on prescription origins and the exploration of classical famous formulas, and promoting dosage form innovation and precise medication to enhance their clinical value.  
    关键词:rheumatoid arthritis;Chinese patent medicine;data mining;prescription analysis;new drug research and development   
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    SONG Shuying, WEN Changqing, XING Luwan, ZHANG Yan, GE Haitao, WANG Fujiang

    DOI:10.13422/j.cnki.syfjx.20260106
    摘要:ObjectiveTo elucidate the mechanism by which total flavonoids of Abelmoschi Corolla (TFA) treat immunoglobulin A (IgA) nephropathy (IgAN) through serum metabolomics analysis.MethodsSPF-grade male SD rats were randomly assigned into six groups (n=10): blank, model, low-dose TFA (TFA-L, 27 mg·kg-1), medium-dose TFA (TFA-M, 54 mg·kg-1), high-dose TFA (TFA-H, 108 mg·kg-1), and losartan potassium (LST, 4.5 mg·kg-1) groups. The remaining five groups, excluding the blank group, were modeled with bovine serum albumin (BSA), lipopolysaccharide (LPS), and carbon tetrachloride (CCl4). Specifically, from weeks 1 to 10, BSA was administered via gavage every other day, and a mixture of castor oil and CCl4 was injected subcutaneously once a week, with LPS injected into the tail vein at weeks 6 and 8. After successful modeling, each intervention group was administrated with the medication prepared with distilled water once daily by gavage for a continuous period of 4 weeks. The levels of 24-hour urinary total protein (24 h UP) and serum creatinine (SCr) were quantified by kits, and the serum IgA level was determined by enzyme-linked immunosorbent assay (ELISA). Renal pathological changes were observed by hematoxylin-eosin (HE) staining and periodic acid-Schiff (PAS) staining. Renal IgA deposition was assessed by immunofluorescence (IF). Endoplasmic reticulum (ER) stress was observed by transmission electron microscopy. Western blot and immunohistochemistry (IHC) were employed to detect the expression of ER stress-related factors. Non-targeted metabolomics was used to screen differential metabolites for analysis, and key metabolites arachidonic acid (AA), prostaglandin E2 (PGE2), and cyclooxygenase-2 (COX-2) were validated.ResultsCompared with the blank group, the model group showed increased 24-hour urine protein (24 h UP) and serum creatinine (SCr) levels (P<0.01), obvious renal pathological damage, elevated serum IgA level (P<0.01), increased renal AA and PGE2 levels (P<0.01), and up-regulated protein levels of COX-2, glucose-regulated protein 78 (GRP78), phosphorylated eukaryotic initiation factor 2α (P-EIF2α), activating transcription factor 4 (ATF4), inositol-requiring enzyme 1α (IRE1α), and spliced X-box binding protein 1 (XBP1s) in the renal tissue (P<0.05, P<0.01). Compared with the model group, the intervention groups showed reductions in 24 h UP and SCr levels (P<0.05, P<0.01), alleviated renal pathological injury, decreased serum IgA level (P<0.05, P<0.01), and reduced renal AA and PGE2 levels (P<0.01). Western blot and IHC results showed that TFA reduced the levels of COX-2, GRP78, P-EIF2α, ATF4, IRE1α, and XBP1s in the renal tissue (P<0.05, P<0.01). Metabolomics results indicated that 51 commonly differential metabolites were found among the normal, model, and TFA-M groups. TFA ameliorated IgAN by affecting metabolic pathways related to the biosynthesis of arachidonic acid and arginine through L-aspartic acid, prostaglandin 2α, leukotriene B4, leukotriene D4, among others.ConclusionTFA can regulate the arachidonic acid metabolism pathway, thereby modulating ER stress, reducing renal damage, and ameliorating IgA nephropathy.  
    关键词:Abelmoschi Corolla total flavonoids;immunoglobulin A (IgA) nephropathy;arachidonic acid metabolism pathway;metabolomics;endoplasmic reticulum stress   
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    更新时间:2026-04-14

    GUO Zhonghao, LI Quan, PAN Pengyu, ZHAO Tengyu, AN Zeyuan, LIU Yuan, ZHOU Yanyan

    DOI:10.13422/j.cnki.syfjx.20251905
    摘要:Parkinson's disease (PD) is a common neurodegenerative disorder characterized by motor impairments, with its pathological mechanisms involving multiple processes such as the degeneration of dopaminergic neurons and the abnormal aggregation of α-synuclein. Current Western medical treatments face challenges including diminished long-term efficacy and motor complications. In recent years, Traditional Chinese Medicine (TCM) has demonstrated advantages in the prevention and treatment of PD through its systematic regulatory capabilities, featuring multi-component, multi-target, and multi-pathway approaches.This article systematically reviews the roles of seven key signaling pathways-NF-κB, AMPK/mTOR, PI3K/Akt, MAPKs, Nrf2/ARE, Wnt/β-catenin, and BDNF/TrkB-in the pathological process of PD and the regulatory mechanisms of TCM. Research indicates that active ingredients of Chinese herbs and compound formulations can synergistically modulate these pathways, exerting comprehensive effects in inhibiting neuroinflammation, alleviating oxidative stress, promoting autophagy to clear abnormal proteins, and enhancing neurotrophic support. These signaling pathways form a complex regulatory network through crosstalk among key nodal molecules, constituting an intricate regulatory system in PD pathology. The multi-target intervention characteristics of TCM align well with this network-based regulatory requirement, achieving integrated anti-inflammatory, antioxidant, autophagy-regulating, and neurorestorative effects through synergistic multi-pathway modulation. This article systematically outlines the mechanisms of TCM in the coordinated regulation of multiple pathways, providing a theoretical basis for elucidating the pathological process of PD and the intervention mechanisms of TCM, while also offering new perspectives and directions for modern research on TCM in the prevention and treatment of PD.  
    关键词:Parkinson's disease;traditional Chinese medicine;signal pathways;mechanism of action;research progress   
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    HAN Ming, ZHANG Ying, KONG Lingya, DAI Jun, ZHANG Ting, MA Zhihong

    DOI:10.13422/j.cnki.syfjx.20251904
    摘要:ObjectiveTo investigate the therapeutic mechanism of Xuefu Zhuyutang (XFZYT) for metabolic-associated fatty liver disease (MAFLD) through integrated network pharmacology and animal experiments.MethodsNetwork pharmacology was utilized to predict the core components, key therapeutic targets, and signaling pathways of XFZYT in the treatment of MAFLD. For animal experiments, a rat model of MAFLD was established by feeding a high-cholesterol diet for 4 weeks. Intervention was then administered with low-dose (2 g·kg-1) and high-dose (4 g·kg-1) XFZYT for 2 weeks. Biochemical assays were performed to measure the serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL). In addition, the activities of superoxide dismutase (SOD) and catalase (CAT) and levels of malondialdehyde (MDA) and glutathione (GSH) in the serum were measured. The same way was adopted to measure the levels of TC and TG in the liver tissue. Enzyme-linked immunosorbent assay (ELISA) was employed to quantify the serum levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor-alpha (TNF-α). Histopathological evaluations included hematoxylin and eosin (HE) staining for liver tissue morphology, Oil Red O staining for lipid deposition, and dihydroethidium (DHE) probe staining for reactive oxygen species (ROS) levels. Western blot analysis was conducted to assess the protein levels of AMP-activated protein kinase (AMPK), phosphorylated (p)-AMPK, nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear factor-kappa B (NF-κB), and p-NF-κB in the liver tissue. Untargeted metabolomics analysis of the serum was performed by liquid chromatography-tandem mass spectrometry (LC-MS/MS).ResultsNetwork pharmacology analysis predicted 155 potential targets of XFZYT for MAFLD treatment, with core targets including signal transducer and activator of transcription 3 (STAT3), protein kinase B1 (Akt1), TNF, and IL-6. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment primarily implicated the AMPK signaling pathway. Animal experiments demonstrated that compared with the normal group, the model group exhibited dyslipidemia, hepatic function impairment, pronounced hepatic lipid deposition, and inflammatory manifestations, with elevated serum levels of AST, ALT, TC, TG, LDL, and MDA (P<0.05), reduced HDL and GSH levels plus decreased SOD and CAT activities (P<0.05), downregulated protein levels of Nrf2, HO-1, and p-AMPK (P<0.05), and upregulated protein level of p-NF-κB (P<0.05) in the liver tissue. Compared with the model group, XFZYT intervention groups showed significant amelioration of dyslipidemia and hepatic function impairment, markedly reduced hepatic lipid deposition and inflammatory cell infiltration, decreased serum levels of AST, ALT, TC, TG, LDL, and MDA (P<0.05), increased HDL and GSH levels plus enhanced SOD and CAT activities (P<0.05), upregulated protein levels of Nrf2, HO-1, and p-AMPK (P<0.05), and downregulated protein level of p-NF-κB (P<0.05). Serum metabolomics revealed 511 differentially expressed metabolites (231 upregulated and 280 downregulated) between normal and model groups, while XFZYT groups versus model group showed 94 differential metabolites (51 upregulated and 43 downregulated). Among them, 11 metabolites displayed the most significant alterations, with enriched pathways including glycerolipid metabolism, cholesterol metabolism, and insulin resistance, multiple of which demonstrated AMPK association.ConclusionXFZYT alleviates MAFLD by regulating the AMPK signaling pathway and associated metabolic networks.  
    关键词:Xuefu Zhuyutang;metabolic-associated fatty liver disease;network pharmacology;metabolomics;AMP-activated protein kinase (AMPK) signaling pathway   
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    更新时间:2026-04-14

    JIANG Fuquan, LIU Tonghua, QIN Lingling, WU Lili, LIU Jingfeng

    DOI:10.13422/j.cnki.syfjx.20260825
    摘要:ObjectiveTo investigate the protective effects and molecular mechanisms of Qiqiao Qingwen Jiedu Granules (QQQW) against viral pneumonia induced by H1N1 influenza virus infection in mice.MethodsThirty-six male Balb/c mice were randomly assigned to six groups (n = 6 per group), i.e., blank control, model, QQQW low-dose (1.25 g·kg-1), QQQW medium-dose (2.5 g·kg-1), QQQW high-dose (5 g·kg-1), and oseltamivir (20 mg·kg-1). Except for the blank control, mice in the remaining groups were intranasally inoculated with H1N1 virus at 1.5 × LD50 to establish a pneumonia model. Drug administration began 2 hours after infection, once daily for 7 consecutive days, and relevant indicators were assessed 24 hours after the final dose. Lung pathological damage was evaluated using hematoxylin-eosin (HE) staining combined with histopathological scoring. Liquid chromatography-mass spectrometry (LC-MS) was used to identify blood-absorbed prototype components, and network pharmacology was applied to predict core targets and signaling pathways. Human non-small cell lung cancer A549 cells were used for in vitro verification, including CCK-8 assay, flow cytometry for apoptosis, and Western blot.ResultsCompared with the blank control, the model group showed significant increases in lung and spleen indices, lung pathological scores, and serum interleukin (IL)-17, IL-6, IL-1β, and tumor necrosis factor (TNF)-α levels (P<0.01), along with significant decreases in phosphorylated phosphatidylinositol 3-kinase (p-PI3K)/PI3K, phosphorylated protein kinase B (p-Akt)/Akt, and phosphorylated glycogen synthase kinase 3β (p-GSK3β)/GSK3β ratios in lung tissue (P<0.01). All QQQW dose groups significantly reduced organ indices, pathological scores, and pro-inflammatory cytokine levels (P<0.05), with the high-dose group showing effects comparable to oseltamivir. The high-dose QQQW group significantly upregulated phosphorylated protein ratios in the PI3K/Akt/GSK3β pathway (P<0.01). In A549 cells, 100 mg·L-1 QQQW significantly increased cell viability, decreased apoptosis, and upregulated phosphorylated protein ratios in this pathway compared with the H1N1 infection model group (P<0.01). These effects were reversed by the PI3K inhibitor LY294002 (P<0.01). Network pharmacology analysis identified GSK3β as a key target and PI3K/Akt as the core pathway of QQQW.ConclusionQQQW (1.25-5 g·kg-1) dose-dependently alleviates H1N1-induced lung inflammation and tissue damage by activating the PI3K/Akt/GSK3β signaling pathway. The high dose (5 g·kg-1) shows comparable efficacy to oseltamivir (20 mg·kg-1).  
    关键词:Qiqiao Qingwen Jiedu Granules;H1N1 influenza virus;phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase 3β (GSK3β) signaling pathway;lung injury;network pharmacology   
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    SUN Zijin, ZHANG Haojia, WANG Kai, WANG Zhaoyi, SONG Linjing, XU Wenxiu, JI Jing, LI Changxiang, WANG Qingguo, WANG Xueqian, CHENG Fafeng

    DOI:10.13422/j.cnki.syfjx.20260124
    摘要:ObjectiveTo investigate the regulatory effects of Huanglian Jiedu decoction (HLJD) on immune cell migration, blood-brain barrier protection, and cellular functional recovery in a model of ischemic stroke.MethodsA transient middle cerebral artery occlusion (tMCAO) model was established in mice to induce ischemic stroke. Cerebral blood flow and neurological function were evaluated using laser speckle imaging and neurological deficit scoring. Histopathological damage in brain tissues was assessed by hematoxylin-eosin (HE) and Nissl staining. Mice were divided into a sham group, a model group, an HLJD group, and a Ginkgo biloba extract (GBE) group. After one week of acclimatization, intragastric administration was initiated. The sham and model groups received normal saline, the HLJD group received HLJD at 1.82 g·kg-¹, and the GBE group received GBE at 0.432 g·kg-¹. Administration was continued for 5 consecutive days, and the tMCAO model was established after the final dose on day 6. Single-cell RNA sequencing was performed on brain tissues and peripheral immune cells. UMAP and odds ratio (OR) indices were used to analyze cell distribution. Differential expression analysis was conducted to evaluate the effects of HLJD on endothelial cells, pericytes, and macrophages, combined with CellChat and decoupler to analyze cell-cell communication and transcription factor regulation. Finally, PCR and ELISA were used to validate the mRNA and protein expression of relevant genes.ResultsCompared with the sham group, the model group showed significantly increased neurological deficit scores (P<0.01) and significantly decreased cerebral blood flow (P<0.01), accompanied by cortical structural disorder, aggravated cytoplasmic vacuolization, and increased numbers of Nissl bodies. Compared with the model group, both the HLJD and GBE groups exhibited significantly reduced neurological deficit scores (P<0.01) and markedly improved cerebral blood flow (P<0.01), along with amelioration of cortical structural disorder, alleviated cytoplasmic vacuolization, and reduced numbers of Nissl bodies. Single-cell analysis showed that HLJD protected endothelial cells and pericytes by preventing their reduction, restored the expression of functional genes in these cells (e.g., PECAM1 and NOS3), and downregulated the expression of chemokines and adhesion-related factors (e.g., CCL2 and CXCL2). In macrophages, HLJD reduced their recruitment to the central nervous system and downregulated the expression of chemokine receptors and inflammatory factors (e.g., IL-6, CCR2, and CXCR2). Cell-cell communication analysis further indicated that HLJD, through the above mechanisms, alleviated damage to pericytes and endothelial cells, reduced their recruitment of macrophages, and decreased ligand-receptor interactions in chemokine signaling pathways (including CCL, CXCL, and CSF3) between pericytes/endothelial cells and macrophages, thereby preventing secondary injury. Compared with the sham group, the model group showed significantly upregulated mRNA expression levels of IL-1β, IL-6, TNF-α, CCL2, CXCL2, and CSF3 (P<0.01), while mRNA expression levels of endothelial- and pericyte function-related genes (RGS5, PECAM1, VEGFB, and NOS3) were significantly downregulated (P<0.01). In contrast, compared with the model group, the HLJD and GBE groups exhibited significantly decreased mRNA expression levels of IL-1β, IL-6, TNF-α, CCL2, CXCL2, and CSF3 (P<0.01), and significantly increased expression of RGS5, PECAM1, VEGFB, and NOS3 (P<0.01). At the protein level, compared with the sham group, the model group showed significantly increased expression of IL-1β, IL-6, and TNF-α (P<0.01), whereas these protein levels were significantly reduced in the HLJD and GBE groups compared with the model group (P<0.01).ConclusionHLJD reduces neuronal damage in ischemic stroke by protecting endothelial cells and pericytes, while inhibiting their interaction with macrophages, thereby mitigating secondary injury in the central nervous system.  
    关键词:Huanglian Jiedu Decoction;ischemic stroke;single-cell transcriptomics;central-peripheral interaction   
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    ZHANG Haojia, WANG Kai, LIU Kunjing, LAN Xin, SUN Zijin, WANG Chunyu, MA Wenyuan, SHAO Wei, HAN Jinhua, DONG Liyang, LI Changxiang, WANG Xueqian, CUI Youxiang, CHENG Fafeng, WANG Qingguo

    DOI:10.13422/j.cnki.syfjx.20260326
    摘要:ObjectiveTo investigate whether Huanglian Jiedutang (HLJD) and its major active constituents (geniposide, baicalin, and berberine) can inhibit the inflammatory response of BV2 cells under lipopolysaccharide (LPS) stimulation via the high-mobility group protein B1 (HMGB1)/Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway, and to explore differences in therapeutic efficacy among the three monomers, their combined formula, and HLJD under equal content ratios.MethodsBV2 microglial cells were used as the primary experimental model. Cell viability was assessed using the cell counting kit-8 (CCK-8) method to examine the effects of different concentrations of dimethyl sulfoxide (DMSO, 0.8%, 0.4%, 0.2%, 0.1%, and 0.05%) on cell viability. IncuCyte was employed to monitor the growth of cells under different concentrations of HLJD (200, 100, 50, 25, 12.5, and 6.25 mg·L-1). Nitric oxide (NO) assay was used to screen the optimal HLJD concentration. High-performance liquid chromatography (HPLC) determined the content of geniposide, baicalin, and berberine in HLJD, and experimental groups were subsequently established according to the relative proportions of these constituents. CCK-8 assay evaluated cell viability under different treatments. Enzyme-linked immunosorbent assay (ELISA) measured levels of inflammatory factors (TNF-α, IL-1β, IL-6, IL-10) in the supernatant. Flow cytometry assessed the effects of treatments on M1-type polarization of BV2 cells. Western blot determined the expression levels of HMGB1, TLR4, and NF-κB-related proteins.ResultsCompared with the blank group, DMSO at concentrations ≤0.2% did not affect cell viability within 48 h. BV2 cell growth plateaued at 24 h after treatment with 200 mg·L-1 HLJD. Under stimulation with 2 mg·L-1 LPS, this concentration of HLJD effectively reduced NO release, and 6 h pre-treatment had a stronger inhibitory effect on NO than direct administration. HPLC results showed that 1 mg of HLJD freeze-dried powder contained approximately 24 μg of geniposide, 15 μg of baicalin, and 30 μg of berberine. Based on these ratios, experimental groups were blank, LPS (2 mg·L-1), HLJD (200 mg·L-1), monomer combination, geniposide (4.8 mg·L-1), baicalin (3 mg·L-1), and berberine (6 mg·L-1). The monomer combination group consisted of all three active constituents dissolved together. LPS and HLJD or its active constituents did not affect cell viability compared with the blank group. LPS significantly increased TNF-α, IL-1β, IL-6, and IL-10 in the supernatant (P<0.01). HLJD and its active constituents significantly reduced pro-inflammatory factors TNF-α, IL-1β, and IL-6 (P<0.05, P<0.01) while upregulating anti-inflammatory IL-10 (P<0.01), with the monomer combination showing the strongest effect (P<0.05, P<0.01). Compared with the blank group, LPS significantly increased the proportion of CD80⁺CD86⁺ (M1-type) BV2 cells (P<0.01). HLJD and its constituents partially inhibited M1 polarization (P<0.05, P<0.01), with the monomer combination exhibiting the most pronounced effect (P<0.05, P<0.01). Compared with the blank group, LPS upregulated HMGB1, TLR4, and NF-κB-related proteins (P<0.01), whereas HLJD and its active constituents significantly reduced their expression (P<0.05, P<0.01), with the monomer combination having the strongest regulatory effect (P<0.05, P<0.01).ConclusionHLJD and its major active constituents (geniposide, baicalin, berberine) can inhibit LPS-induced inflammatory responses in BV2 cells. The combination of the three active constituents demonstrates the most potent anti-inflammatory effect, significantly attenuating M1-type polarization of BV2 cells via the HMGB1/TLR4/NF-κB signaling pathway.  
    关键词:Huanglian Jiedutang;HPLC detection;BV2 microglia cells;M1-type polarization;high-mobility group protein B1 (HMGB1)/Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway   
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    SUN Mengying, WANG Lizhen, LI Tong, WANG Leilei, JIA Shiyan, WANG Tingting, YANG Yanwen, SI Kaiqiang, CUI Youxiang, LIU Zhilong

    DOI:10.13422/j.cnki.syfjx.20260523
    摘要:ObjectiveTo investigate the effects of Huanglian Jiedu Tang (HLJD) on cognitive function in mice with ischemic stroke (IS) and to elucidate whether its neuroprotective effects are mediated by inhibition of the nuclear factor κB (NF-κB) signaling pathway and subsequent suppression of NF-κB-regulated neuronal apoptosis.MethodsAn IS model was established using middle cerebral artery occlusion (MCAO). Sixty C57BL/6J mice were randomly assigned to five groups (n = 15 per group), i.e., sham operation, model, HLJD low-dose (3.9 g·kg-1·d-1), HLJD high-dose (7.8 g·kg-1·d-1), and Ginkgo biloba extract (GBE, 31.2 mg·kg-1·d-1). Post-operatively, neurological deficit scores (Longa score), cerebral infarct volume assessed by 2,3,5-triphenyltetrazolium chloride (TTC) staining, and brain water content were evaluated. Learning and memory were assessed using new object recognition (NOR) and fear conditioning (FC) tests. Hippocampal pathology was examined via hematoxylin and eosin (HE) staining. Immunofluorescence detected expression of glial fibrillary acidic protein (GFAP, astrocyte marker), cellular oncogene Fos (c-Fos, neuronal activation marker), and glutamate decarboxylase 65 (GAD65, γ-aminobutyric acid-synthesizing enzyme). Western blot measured nuclear factor κB inhibitor protein α (IκBα), phosphorylated IκBα (p-IκBα), NF-κB p65, phosphorylated NF-κB p65 (p-NF-κB p65), ionic calcium binding adapter molecule 1 (Iba-1), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and apoptosis-related proteins, such as cleaved cysteinyl aspartate-specific protease 3 (Caspase-3), B-cell lymphoma 2 (Bcl-2), and Bcl-2-associated X protein (Bax). Real-time quantitative PCR (Real-time PCR) was used to assess mRNA levels of Iba-1, TNF-α, IL-1β, NF-κB p65, cleaved Caspase-3, Bax, and Bcl-2.ResultsCompared with the sham group, the model group exhibited significantly increased neurological deficit scores, brain water content, and cerebral infarct volume (P<0.01). Hippocampal CA1 neurons were disorganized, showing nuclear pyknosis and karyolysis. NOR exploration time and FC freezing time were significantly reduced (P<0.01). GFAP and c-Fos expression were increased, while GAD65 expression was decreased (P<0.01). Cleaved Caspase-3 and Bax were upregulated, Bcl-2 was downregulated, and the Bax/Bcl-2 ratio was elevated (P<0.01). Expression levels of p-IκBα, p-NF-κB p65, IL-1β, TNF-α, and Iba-1 were significantly increased (P<0.01). Compared with the model group, HLJD high-dose, low-dose, and GBE groups showed significant improvements in all parameters (P<0.01). Among them, the HLJD high-dose group showed the most pronounced neuronal structural recovery and superior performance in NOR and FC tests (P<0.01). In this group, GFAP and c-Fos decreased, GAD65 increased (P<0.01), apoptosis-related protein expression was reversed, and NF-κB signaling and related inflammatory factor expression were suppressed (P<0.01).ConclusionHLJD ameliorates cognitive dysfunction in mice after IS, potentially by inhibiting the NF-κB signaling pathway, thereby reducing neuroinflammation and hippocampal neuronal apoptosis.  
    关键词:Huanglian Jiedu Tang;ischemic stroke;NF-κB signaling pathway;neuroinflammation;apoptosis;cognitive impairment;hippocampus   
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    DONG Liyang, ZHANG Qinyuan, WU Yiping, HE Yingping, SHAO Wei, ZHANG Haojia, WANG Xueqian, LI Changxiang, CUI Youxiang, CHENG Fafeng, WANG Qingguo

    DOI:10.13422/j.cnki.syfjx.20260921
    摘要:Huanglian Jiedu Tang (HLJDT), as a classical formula for clearing heat and removing toxins, has been widely applied in the treatment of various clinical diseases in recent years, particularly during the fire-heat stage of stroke, where it has attracted considerable attention. Based on previous studies, this paper systematically elaborates on the research progress on the active components of HLJDT, its clinical application in ischemic stroke, and advances in studies on its mechanisms of action. Modern pharmacological studies have demonstrated that HLJDT contains multiple active components, including baicalin, geniposide, and berberine. In the treatment of ischemic stroke, these components exert therapeutic effects through multi-target, multi-pathway, and multi-level mechanisms. Clinical studies have shown that HLJDT can increase cerebral blood flow, reduce cerebral infarct volume, and improve post-stroke physical dysfunction in patients with ischemic stroke. Experimental studies have indicated that HLJDT can improve neurological function scores and increase cerebral perfusion in experimental stroke models. In addition, the mechanisms underlying the anti-ischemic stroke effects of HLJDT may be related to anti-inflammatory and antioxidant activities, promotion of angiogenesis, and regulation of amino acid and energy metabolism. Although existing studies have confirmed that HLJDT exhibits multi-target and multi-pathway synergistic therapeutic characteristics, further large-sample randomized controlled trials are still needed to verify its long-term efficacy and to further elucidate the dynamic interaction network among components, targets, and pathways. Combined with network pharmacology and molecular docking analyses, this study further clarifies the synergistic targets of the core components (berberine, baicalin, and geniposide), providing a theoretical basis for in-depth research and clinical translation of HLJDT in the treatment of ischemic stroke.  
    关键词:Huanglian Jiedu Tang;ischemic stroke;active ingredient;clinical application;experimental research;multi-target regulation   
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    ZHANG Zeming, LIU Lanchun, LI Qiyang, SUN Xuan, ZHANG Ruoqi, ZHANG Yiyao, WANG Jie

    DOI:10.13422/j.cnki.syfjx.20260262
    摘要:Angiogenesis, as a core mechanism for maintaining tissue perfusion and repairing ischemic injury, plays a crucial role in ischemic diseases such as coronary heart disease and peripheral arterial disease. Traditional Chinese medicine(TCM), with its advantages of multi-target and synergistic regulation, provides a unique perspective for therapeutic angiogenesis. Based on this, this article intends to delve into the synergistic effects of key signaling pathways, including vascular endothelial growth factor(VEGF)/VEGF receptor(VEGFR), Notch, phosphoinositide 3-kinase/ protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR), and angiopoietin/endothelial TEK tyrosine kinase(Ang/Tie2), and elucidate the driving mechanisms of endothelial cell metabolic reprogramming and exosome-mediated intercellular communication within this process. Based on existing literature, it summarizes the microenvironment-dependent and bidirectional regulatory characteristics of natural active components of TCM(such as terpenes, tanshinones, and flavonoids) on angiogenesis. Furthermore, it systematically discusses how classical TCM formulas achieve blood vessel formation and functional maturation by protecting the neurovascular units, recruiting pericytes, and remodeling the microenvironment. Current evidence highlights the advantages of multi-target synergy and temporal regulation in TCM, but also reveals challenges such as high heterogeneity and a lack of functional evaluations and high-quality clinical trials. Future efforts should integrate multi-omics to decipher network mechanisms, optimize formula compatibility, and conduct multicenter studies to promote the development of innovative preparations. This review highlights the academic value of TCM in angiogenesis, provides an evidence base for treating ischemic diseases, and supports multidisciplinary integration and innovation.  
    关键词:angiogenesis;bidirectional regulation;ischemic diseases;signaling pathways;traditional Chinese medicine;multi-channel collaboration   
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    LI Shiyi, CHENG Hao, JI Chunyan, SUN Jun, XUE Juan

    DOI:10.13422/j.cnki.syfjx.20260168
    摘要:Hepatocellular carcinoma (HCC), as one of the common malignant tumours, has seen a continuous rise in incidence and mortality worldwide, posing a serious threat to human health, and traditional treatments have certain limitations. Therefore, exploring new therapeutic strategies is particularly urgent. In recent years, with in-depth research on the regulatory mechanisms of microRNAs (miRNAs) in tumour occurrence and development, they have become new targets for HCC diagnosis and treatment. As a traditional treatment method, Chinese medicine, due to its multi-component, multi-pathway, and multi-target overall regulatory characteristics, shows broad prospects in treating HCC by regulating miRNAs. Accordingly, this paper reviews recent studies on the role of miRNAs in HCC and research advances in traditional Chinese medicine interventions, finding that various miRNAs play key roles in HCC cell cycle regulation, proliferation and apoptosis, invasion and metastasis, immune microenvironment, and drug resistance. It summarises how active ingredients, extracts, drug pairs, and compound formulations of Chinese medicine act on specific miRNAs to regulate their downstream target gene expression, affecting the malignant behaviour of HCC cells and exerting anti-cancer effects. This study aims to provide a theoretical basis for miRNAs as potential biomarkers and therapeutic targets for HCC, as well as to offer new ideas for developing miRNA-based targeted Chinese medicine therapies.  
    关键词:hepatocellular carcinoma;microRNA;active constituents;herb pair;traditional Chinese medicine formulas   
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    LYU Tengfei, WANG Jingyu, XIE Mingyue, XI Bin

    DOI:10.13422/j.cnki.syfjx.20250612
    摘要:ObjectiveBased on 16S rDNA technology and molecular biology methods, the molecular mechanism of Shenling Baizhu San in the treatment of diarrhea-predominant irritable bowel syndrome (IBS-D) was investigated.MethodsThe 42 SD rats with SPF were randomly divided into no control group, SLBZS-H, medium (SLBZS-M), low (SLBZS-L) dose group, positive control group and model group, with 7 rats in each group. The rat model of IBS-D was prepared by ice-cold senna (0.45 g∙mL-1) gavage (0.01 mL∙g-1) combined with restraint stress for 14 consecutive days. After successful modeling, the corresponding drugs were given to each group with a gavage volume of 0.01 mL∙g-1: The positive group was administered with 2.36 , 1.18 and 0.59 g∙mL-1 of Shenling Baizhu San in the Positive group and the Model group with the same volume of normal saline for 14 d. The general condition of the rats: Weight, feces, mental state and death were observed and recorded. The body weight, abdominal wall retraction reflex score (AWR) and loose stool rate of rats in each group were measured before (the first day), after the model (day 14) and after treatment (day 28). Hematoxylin-eosin staining was used to observe the morphological characteristics of colon tissues of experimental animals. Enzyme-linked immunosorbent assay was used to quantitatively analyze the concentration of inflammatory mediators in the peripheral blood of experimental animals. Western blotting was used to detect the expression levels of key proteins of Toll-like receptor 4 (TLR4), Toll-like receptor 2 (TLR2), myeloid differentiation factor 88 (MyD88) and nuclear factor-κB (NF-κB) signaling pathway in rat colon tissue. 16S rDNA technology was used to detect the structural changes of intestinal microbiota in rats.ResultsCompared with Control, the colon of the Model group showed partial mucosal epithelial shedding and inflammatory cell infiltration. The contents of TNF-α, IL-1β, IL-6 and 5-HT in serum increased (P<0.05), the protein expressions of TLR2, TLR4, MYD88 and NF-κB in colon tissue increased (P<0.05), the diversity indices of Richness, Chao1, abundance-based coverage estimator(ACE) and Shannon decreased (P<0.05), and the phylum Firmicutes, Actinobacteria, The relative richness of Bacteroides-H, Lactobacillus and Ligilactobacillus decreased (P<0.05), while the relative richness of Bacteroidetes, Proteobacteria and Prevotella increased (P<0.05). Compared with the model group, the colonic structure and organization of the SLBZS-H group, SLBZS-M group, SLBZS-L group and Positive group were clearer, and only a small number of inflammatory cells were present in some areas, and the serum contents of TNF-α, IL-1β, IL-6 and 5-HT were decreased (P<0.05), TLR2, TLR4, The protein expressions of MyD88 and NF-κB decreased (P<0.05), and compared with the model group, the diversity indices of Richness, Chao1, ACE and Shannon in the SLBZS-H, SLBZS-M and SLBZS-L groups increased (P<0.05), and the richness of Firmicutes and Actinobacteria increased (P<0.05). The richness of Proteobacteria and Prevotella decreased (P<0.05), and the abundance of Prevotella decreased (P<0.05), Bacteroides-H, Muribaculum, Lactobacillus and Lactobacillus in the Positive group salivarius (P<0.05).ConclusionShenling Baizhu San can effectively treat IBS-D, and its molecular mechanism may be to play a therapeutic role by improving intestinal flora and inhibiting the TLRS/MyD88/NF-κB signaling pathway to reduce inflammatory response.  
    关键词:Shenling Baizhu San;diarrhoeal irritable bowel syndrome;intestinal flora;immune inflammation;toll-like receptors/myeloid differentiation factor 88/nuclear factor-κB(TLRs/MyD88/NF-κB)   
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    HE Youcheng, JIANG Fengru, WANG Yanru, HUANG Minghan, WU Yue, ZHOU Chunyu, MO Lian, WEI Lifeng, PAN Keyi, CAI Shuyu, YUAN Jianye

    DOI:10.13422/j.cnki.syfjx.20250512
    摘要:Both cathartic colon (CC) and cathartic-dependent constipation (CDC) are caused by the abuse of stimulant laxatives, while their concepts are not completely the same.Starting from the disease name of CC, this article traced the origin and evolution of the concept of CC, summarizes and compared the similarities and differences between CC, CDC, and slow transit constipation (STC), and called for strict differentiation among the three.Furthermore, this article explored the specific contents of Western medicine clinical subtypes and traditional Chinese medicine (TCM) syndrome differentiation of CDC and delved into the TCM pathogenesis of CDC according to both literature and clinical practice.The relationship between clinical subtypes and TCM syndromes was established, and the syndrome characteristics of CDC of different clinical subtypes and TCM syndromes were summarized.The recommended prescriptions for corresponding syndromes were listed.A systematic CDC diagnosis and treatment approach of "clinical subtypes-syndrome differentiation-syndrome characteristics-recommended prescriptions" was thus formed.Additionally, the paper provides an overview of current research on CDC in both Western medicine and TCM contexts, identifies future research directions, and suggests research pathways for refining and advancing CDC studies.  
    关键词:cathartic colon;cathartic-dependent constipation;clinical subtype;syndrome differentiation   
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    HE Youcheng, SHAN Jingyi, JIANG Fengru, WU Yue, ZHOU Chunyu, HANG Lu, ZHOU Yan, MO Lian, CAI Shuyu, PAN Keyi, WEI Lifeng, YUAN Jianye

    DOI:10.13422/j.cnki.syfjx.20251718
    摘要:ObjectiveTo observe the clinical efficacy of the Yiqi Yangyin Huoxue formula (YYHF) in the treatment of cathartic colon (CC) and its effects on fecal short-chain fatty acids (SCFAs), and to explore the correlations among CC severity indicators and between these indicators and patient history.MethodsAccording to the inclusion and exclusion criteria, 98 patients meeting the diagnostic criteria of both traditional Chinese and Western medicine for CC with the syndrome of Qi-Yin deficiency complicated by blood stasis were randomly assigned to an observation group and a control group. The observation group received YYHF granules, while the control group received lactulose. Both medications were administered twice daily, one sachet each time, half an hour after breakfast and dinner, with a treatment course of 8 weeks. The primary constipation symptom score, Patient Assessment of Constipation Quality of Life (PAC-QOL) score, and TCM syndrome score were assessed before and after treatment and at the 8th week after the end of treatment. The overall clinical effective rate, as well as the efficacy attenuation index and degree, were evaluated. Fecal SCFA levels were measured using gas chromatography-mass spectrometry (GC-MS). Spearman correlation analysis was performed to explore the correlations among CC severity indicators and between these indicators and patient history.ResultsThe overall clinical effective rate in the observation group (95.83%) was higher than that in the control group (78.72%) (P<0.05). After treatment, the total scores for primary constipation symptoms, PAC-QOL, and TCM syndromes decreased in both groups (all P<0.05), with more significant reductions in the observation group (P<0.05). The severity of all primary constipation symptoms was alleviated in both groups (all P<0.05). In terms of "excessive straining and difficult defecation", "anal heaviness, incomplete evacuation, and bloating sensation", "abdominal distension", and "defecation frequency", the observation group showed better efficacy than the control group (all P<0.05). Scores of the four PAC-QOL dimensions and the scores and severity of primary and secondary TCM symptoms were reduced in both groups (all P<0.05), with more significant reductions in the observation group (all P<0.05). After treatment, acetic acid, propionic acid, butyric acid, and total SCFAs in the observation group increased significantly (all P<0.05). The efficacy attenuation index and degree in the observation group were lower than those in the control group (all P<0.05). No severe adverse reactions occurred in either group, and there was no statistically significant difference in the incidence of adverse reactions between the two groups. Positive correlations of varying degrees were observed among the total scores of primary constipation symptoms, PAC-QOL, and TCM syndromes, as well as between these scores and the history of stimulant laxative use, disease duration, and age.ConclusionYYHF can effectively alleviate the primary constipation symptoms in CC patients, improve quality of life, and ameliorate TCM syndromes, with good safety. It also has the advantage of a lower rebound degree after drug withdrawal, and its mechanism may be related to increasing fecal SCFA levels. Long-term abuse of stimulant laxatives may aggravate the severity of CC and prolong the disease course.  
    关键词:cathartic colon;constipation;Yiqi Yangyin Huoxue formula;short-chain fatty acids;correlation analysis   
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    HU Yixuan, SONG Suhua, WANG Yu

    DOI:10.13422/j.cnki.syfjx.20241719
    摘要:Dabuyuanjian is one of the classic famous formulas in the Catalog of Ancient Classic Famous Formulas (Second Batch)-Medicine of Han Ethnic Group. It consists of Ginseng Radix et Rhizoma, Dioscoreae Rhizoma, Rehmanniae Radix Praeparata, Eucommiae Cortex, Angelicae Sinensis Radix, Corni Fructus, Lycii Fructus, and Glycyrrhizae Radix et Rhizoma Praeparata cum Melle, and is used to treat the symptoms of men and women who have a great loss of Qi and blood and a critical and dramatic loss of spiritual guardianship. This study reviewed the ancient and modern literature, and used literature tracing and bibliometrics methods to mine the key information of the historical origin, formula name, drug composition, compatibility, drug dosage, original plants and processing of drugs, decocting method, and clinical application of Dabuyuanjian. The results showed that Dabuyuanjian was first recorded in the Jing Yue's Collected Works (Jing Yue Quan Shu), with the dosage mainly following the original formula. According to the dosage in the Ming and Qing dynasties, the formula is composed of 5.60 g (for mild cases)/39.17 g (for severe cases) Ginseng Radix et Rhizoma, 7.46 g Dioscoreae Rhizoma, 9.32 g (for mild cases)/ 93.25 g (for severe cases) Rehmanniae Radix Praeparata, 7.46 g Eucommiae Cortex, 9.32 g Angelicae Sinensis Radix, 3.73 g Corni Fructus, 9.32 g Lycii Fructus, and 5.60 g Glycyrrhizae Radix et Rhizoma Praeparata cum Melle. Regarding the original plants of drugs, Ginseng Radix et Rhizoma is produced from the dried roots and rhizomes of Panax ginseng, Dioscoreae Rhizoma from stir-fried dried rhizomes of Dioscorea opposita, Rehmanniae Radix Praeparata from steamed dried roots of Rehmannia glutinosa, Eucommiae Cortex from the dried bark of E. ulmoides, Angelicae Sinensis Radix from the dried roots of Angelica sinensis, Corni Fructus from the dried mature fruit flesh of Cornus officinalis, Lycii Fructus from the dried mature fruits of Lycium barbarum, and Glycyrrhizae Radix et Rhizoma Praeparata cum Melle from the honey-processed dried roots and rhizomes of Glycyrrhiza uralensis. These medicinal materials are decocted in 400 mL water to reach a volume of 140 mL, and the decoction should be taken 1 h after meals, 2-3 bags per day. Dabuyuanjian has a wide range of clinical applications, including gynecological and obstetrical diseases, deficiency, baffling and panic, consumptive thirst, and blood, ear, nose, and throat diseases. In modern clinical practice, it is mainly used for diseases of the nervous system, gynecology, urinary system, cardiovascular system, digestive system, musculoskeletal system, connective tissue, immune system, blood, and men. Through the review of ancient and modern literature, this study sorted out the historical evolution and mined the key information of Dabuyuanjian, aiming to provide a theoretical reference for safe and effective clinical application and subsequent research and development of this formula.  
    关键词:classic famous formula;Dabuyuanjian;ancient books of traditional Chinese medicine;modern application;textual research   
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    HE Youcheng, JIANG Fengru, WU Yue, ZHOU Chunyu, LIU Erhao, ZHOU Pengfei, PAN Keyi, CAI Shuyu, YUAN Jianye

    DOI:10.13422/j.cnki.syfjx.20250314
    摘要:ObjectiveTo evaluate and analyze the syndrome characteristics of Qi and Yin deficiency accompanied by Qi stagnation and blood stasis in a rhein-induced cathartic colon (CC) rat model.MethodsTwenty-four rats were divided into a normal group and a model group (CC group). The rats were administered equal volumes of physiological saline or 2% rhein suspension by gavage to establish the model over three cycles (approximately 118 days). The first cycle lasted 46 days, with a dosage of 1.2 mL·(100 g·d)-1, administered every other day. The second cycle lasted 37 days, with a dosage of 1.2 mL·(100 g·d)-1, administered for 5 consecutive days followed by 2 days of cessation. The third cycle lasted 35 days, with a dosage of 1.6 mL·(100 g·d)-1, also administered for 5 consecutive days followed by 2 days of cessation. Each cycle ended when 80% of the rats no longer exhibited loose stools. Body mass, 24 h food intake, coat condition, and coat red (R), green (G), and blue (B) values were recorded. The open field test (OFT) was used to measure the total distance traveled to evaluate Qi deficiency. The body mass coefficient and 24 h water intake were recorded to assess Yin deficiency. The sucrose preference test (SPT) was used to determine the sucrose preference rate (SPR), and the average speed in OFT was measured to evaluate depressive status (liver depression and Qi stagnation). Tongue images and their R, G, and B values were recorded. Whole blood viscosity (WBV) and plasma viscosity (PV) were measured using an automatic hemorheological analyzer to evaluate blood stasis. A carbon ink propulsion test was performed to determine the intestinal transit rate (ITR) for disease model evaluation. Hematoxylin-eosin (HE) staining was used to observe histopathological changes in the colon. Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) was used to detect the mRNA expression of transient receptor potential ankyrin 1 (TRPA1) and tryptophan hydroxylase 1 (TPH1) in colon tissue. Western blot was used to detect the protein expression of TRPA1 and TPH1.ResultsIn terms of syndrome indicators, compared with the normal group, the body mass of the CC group decreased (P<0.05), while 24 h food intake increased (P<0.01). The coats of the CC group appeared withered, disheveled, and dull, and the R, G, and B values of the coat decreased (P<0.01). The total distance traveled in OFT decreased (P<0.01). The body mass coefficient decreased (P<0.01), while 24 h water intake increased (P<0.05, P<0.01). The SPR decreased (P<0.01), and the average speed in OFT slowed (P<0.01). The tongue appeared dark red, and the R, G, and B values of tongue images decreased (P<0.01). WBV and PV increased (P<0.01). Regarding disease indicators, compared with the normal group, the ITR decreased in the CC group (P<0.01). Pathologically, HE staining showed necrosis and shedding of colonic mucosal epithelial cells, disruption of mucosal continuity, and infiltration of inflammatory cells in the lamina propria in the CC group. Semi-quantitative analysis showed increased HAI scores (P<0.05) and increased inflammatory cell counts and area proportion (P<0.05). In terms of molecular biological indicators, compared with the normal group, the mRNA and protein expression levels of TRPA1 and TPH1 in colon tissue decreased in the CC group (P<0.05, P<0.01).ConclusionThe rhein-induced CC rat model conforms to the traditional Chinese medicine syndrome characteristics of Qi and Yin deficiency accompanied by Qi stagnation and blood stasis.  
    关键词:cathartic colon;animal model;syndrome of traditional Chinese medicine;deficiency of Qi and Yin;Qi stagnation and blood stasis   
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    HE Youcheng, LIN Shijin, JIANG Fengru, LI Sihan, KE Xiao, WANG Wenrong, YUAN Jianye, Huang Minghan

    DOI:10.13422/j.cnki.syfjx.20251812
    摘要:Functional constipation (FC) is a clinically common functional bowel disorder characterized by a protracted course and associations with various chronic disorders and psychological abnormalities. Although not life-threatening, FC significantly impairs patients' quality of life. FC subtypes include slow-transit constipation (STC), defecatory disorder (DD), and normal-transit constipation (NTC). The pathological mechanisms underlying FC have not been fully elucidated, and overall clinical efficacy remains unsatisfactory. Animal models of FC serve as essential tools for the study of disease mechanisms and the development of novel therapeutics. This article systematically reviews the current state of research on the animal models of FC and identifies that rodents, particularly rats and mice, are the most commonly used species. Dogs and pigs are also employed in complex intervention studies due to their physiological similarities to humans, though their use is limited by housing challenges and ethical considerations. Induction methods vary across different FC subtypes. STC models are primarily established with chemical agents such as loperamide or compound diphenoxylate. DD modeling often involves low-fiber diets combined with methylene blue injection or rectal narrowing. NTC modeling mainly relies on low-fiber dietary interventions. In addition, disease-syndrome combination models based on traditional Chinese medicine (TCM) theory have been developed, encompassing excess patterns such as heat accumulation, cold accumulation, and Qi stagnation, as well as deficiency patterns including Qi deficiency, blood deficiency, Yin deficiency, and Yang deficiency. These are achieved through an approach of disease model + syndrome induction, enabling the integration of mechanisms from both Western and TCM perspectives. Models are evaluated from two aspects: disease and syndrome manifestations (e.g., colonic transit, secretory function, and TCM syndrome indicators such as mental state and body weight) and disease mechanisms (e.g., enteric nervous system, interstitial cells of Cajal, smooth muscle cells, gut microbiota, and metabolites). However, current research still faces challenges such as poor consistency in some models, non-specific interference in mechanism interpretation, insufficient studies on NTC, and lack of TCM tongue and pulse diagnosis in evaluation. Future efforts should focus on optimizing model stability and specificity to provide a more reliable experimental basis for investigating the pathological mechanisms of FC and developing therapeutic agents.  
    关键词:functional constipation;animal models;slow-transit constipation;defecatory disorder;normal-transit constipation;disease-syndrome combination model   
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    更新时间:2026-04-14
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