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Buzhong Yiqitang Combined with Cisplatin Inhibits Lung Adenocarcinoma Cell Proliferation by Suppressing PDK1/Akt Signaling Pathway and Regulating Glycolysis Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the impact of Buzhong Yiqitang combined with cisplatin on the proliferation of human lung adenocarcinoma （A549） cells through regulation of the pyruvate dehydrogenase kinase 1 （PDK1）/protein kinase B （Akt） signaling pathway and influence on glycolysis.MethodsTranscriptome sequencing （RNA-seq） was employed to compare the expression of glycolysis-related genes between A549 cells and cisplatin-resistant human lung adenocarcinoma cells （A549/DDP）. Small interfering RNA （siRNA） was employed to knock down PDK1， and the knockdown efficiency was verified by Western blot and Read-time PCR. The cell counting kit-8 （CCK-8） assay was used to assess the survival and viability of A549 cells under the following conditions： siRNA negative control+cisplatin （128， 64， 32， 16， 8， 4， 0 μmol·L-1）， siPDK1+cisplatin （128， 64， 32， 16， 8， 4， 0 μmol·L-1）， and siPDK1+cisplatin （128， 64， 32， 16， 8， 4， 0 μmol·L-1）+Buzhong Yiqitang （10%）-containing serum. The 20% inhibitory concentration （IC20） of the siRNA negative control+cisplatin group （7.832 μmol·L-1） was calculated and used as the subsequent cisplatin concentration. Colony formation assay was performed to evaluate the proliferation of A549 cells. Lactate and adenosine triphosphate （ATP） assay kits were used to measure lactate and ATP production. The mitochondrial membrane potential was detected with the fluorescent probe JC-1. Western blotting was conducted to examine the expression levels of PDK1， phosphorylated （p）-Akt， Akt， pyruvate kinase M2 （PKM2）， glucose transporter 1 （GLUT1）， pyruvate dehydrogenase （PDH）， and lactate dehydrogenase A （LDHA）. Confocal immunofluorescence was employed to detect PDK1 and p-Akt.ResultsRNA-seq results identified PDK1 as a highly expressed differential gene in glycolysis metabolism between A549 cells and A549/DDP cells， and it was highly expressed in tumor cells. Gene Set Enrichment Analysis （GSEA） revealed upregulated and downregulated genes in glycolysis and gluconeogenesis pathways. Western blot and RT-qPCR confirmed that PDK1-si-2 had the highest transfection efficiency， with a PDK1 knockdown rate exceeding 60%. CCK-8 assay determined the half-maximal inhibitory concentration （IC50） values for each group as （30.698±5.348）， （16.372±3.562）， （13.237±1.573） μmol·L-1， while the IC20 of cisplatin in siRNA negative control-transfected A549 cells was （7.832±0.672） μmol·L-1. Compared with the siRNA negative control group， the siRNA negative control+cisplatin group showed decreased colony formation rate， reduced lactate production， lowered mitochondrial membrane potential， downregulated protein levels of p-Akt， GLUT1， PDK1， PDH， and LDHA， and reduced PDK1 fluorescence intensity （P<0.05）. The siPDK1 group exhibited decreased colony formation rate， reduced lactate production， increased ATP production， lowered mitochondrial membrane potential， downregulated protein levels of p-Akt， PKM2， GLUT1， PDK1， PDH， and LDHA， and reduced PDK1 and p-Akt fluorescence intensity （P<0.05）. Compared with the siPDK1 group， the siPDK1+Buzhong Yiqitang group showed decreased colony formation rate， reduced lactate production， downregulated protein levels of PKM2， GLUT1， and PDK1， and reduced PDK1 fluorescence intensity （P<0.05）. The siPDK1+cisplatin group exhibited decreased colony formation rate， reduced lactate production， increased ATP production， lowered mitochondrial membrane potential， downregulated protein levels of PKM2， GLUT1， PDK1， and PDH， and reduced PDK1 and p-Akt fluorescence intensity （P<0.05）. The siPDK1+cisplatin+Buzhong Yiqitang group demonstrated decreased colony formation rate， reduced lactate production， increased ATP production， lowered mitochondrial membrane potential， downregulated protein levels of p-Akt， PKM2， GLUT1， PDK1， PDH， and LDHA， and reduced PDK1 and p-Akt fluorescence intensity （P<0.05）. Compared with the siPDK1+Buzhong Yiqitang group， the siPDK1+cisplatin group showed decreased colony formation rate， downregulated protein levels of p-Akt and PDH， and reduced PDK1 and p-Akt fluorescence intensity （P<0.05）. The siPDK1+cisplatin+Buzhong Yiqitang group exhibited decreased colony formation rate， reduced lactate production， increased ATP production， lowered mitochondrial membrane potential， downregulated protein levels of p-Akt， GLUT1， PDH， and LDHA， and reduced PDK1 and p-Akt fluorescence intensity （P<0.05）. Compared with the siPDK1+cisplatin group， the siPDK1+cisplatin+Buzhong Yiqitang group showed decreased colony formation rate， increased ATP production， and downregulated protein levels of p-Akt， PKM2， and LDHA （P<0.05）.ConclusionBuzhong Yiqitang combined with cisplatin can suppress lung adenocarcinoma cell proliferation by modulating glycolysis through the PDK1/Akt signaling pathway.Keywords：Buzhong Yiqitang;cisplatin;glycolysis;pyruvate dehydrogenase kinase 1 （PDK1）/protein kinase B （Akt）;small interfering RNA （siRNA）91|20|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Deciphering Mechanism of Guishen Wan on Learning and Memory in A Sub-acute Aging Mouse Model via Kidney-brain Axis Enhanced Publication AI Introduction
Abstract：ObjectiveTo evaluate the Effect of Guishen Wan on learning and memory ability in D-galactose-induced aging model mice and to explore the application of the "Kidney-Brain Coordination" theory in traditional Chinese medicine （TCM）.MethodsAn subacute aging mouse model was established by subcutaneous injection of D-galactose （200 mg·kg-1·d-1） into the neck and back of KM mice. The mice were then administered GuiShen Wan at high， medium， and low doses （18， 9， 4.5 g·kg-1·d-1） or donepezil（2 mg·kg-1·d-1）， a standard clinical therapeutic agent for Alzheimer's disease， served as the positive control in this study，for 4 consecutive weeks. Learning and memory abilities were evaluated using the Morris water maze. The degree of renal fibrosis was observed via Masson staining. Hippocampal neuron injury was assessed by hematoxylin-eosin（HE） staining. Damage to Nissl bodies in the hippocampus was examined using Nissl staining. The fluorescence expression intensity of Klotho in the hippocampus was detected by immunofluorescence. Western blot was used to detect the protein expression of Klotho in the kidneys， as well as proteins related to the hippocampal inflammatory pathway and inflammatory factor-related signaling pathways.ResultsResults from the water maze test showed that compared with the blank group， the number of platform crossings and the time spent in the target quadrant were significantly decreased in the model group （P<0.01）. Compared with the model group， all dose groups of Guishen Wan significantly increased the number of platform crossings and the time spent in the target quadrant in model mice （P<0.01）.Masson staining results showed that compared with the blank group， the collagen volume fraction was significantly increased in the model group （P<0.01）. Compared with the model group， all dose groups of Guishen Wan significantly reduced the collagen volume fraction in the model group （P<0.01）. Kidney Western blot analysis showed that compared with the blank group， the Klotho protein was significantly decreased in the model group （P<0.01）. Compared with the model group， Guishen Wan elevated the klotho protein （P<0.01）.Neuronal cell count results showed that compared with the blank group， the number of neurons was significantly reduced in the model group （P<0.01）. Compared with the model group， Guishen Wan exhibited a dose-dependent trend in repairing neuronal damage and increasing the number of neuronal cells （P<0.01）.Immunofluorescence intensity results showed that compared with the blank group， the positive expression of Klotho was significantly decreased in the model group （P<0.01）. Compared with the model group， all dose groups of Guishen Wan enhanced Klotho fluorescence expression （P<0.01）.Hippocampal Western blot analysis showed that compared with the blank group， the ratios of interleukin（IL）-1β and IL-6 proteins were significantly increased in the model group （P<0.01）. Compared with the model group， all dose groups of Guishen Wan significantly reduced the ratios of IL-1β and IL-6 proteins（P<0.01）. Compared with the blank group， the ratio of phosphorylated-nuclear transcription factor-κB（p-NF-κB） protein was significantly increased （P<0.01）， while the klotho protein was significantly decreased （P<0.01） in the model group. Compared with the model group， all Guishen Wan groups significantly reduced the p-NF-κB protein （P<0.05， P<0.01） and significantly increased the Klotho protein（P<0.01）.ConclusionGuishen Wan effectively ameliorates D-galactose-induced aging in model mice. Its mechanism of action may be related to upregulating Klotho concentration and inhibiting inflammatory factors associated with the NF-κB signaling pathway.Keywords：Guishen Wan;anti-aging;Klotho;inflammation;learning and memory24|6|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Erchentang Alleivates Depression in Obese Mice by Regulating PPAR Signaling Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveTo observe the therapeutic effect of Erchentang on depression in obese mice and explore the therapeutic mechanism.MethodsC57BL/6J mice were randomized into the control， model， metformin （0.65 g·kg-1）， and low-， medium-， and high-dose （3.35， 6.7， and 13.4 g·kg-1， respectively） Erchentang groups. Gavage was initiated simultaneously with modeling and continued for 28 days. The therapeutic effects of Erchentang were evaluated through behavioral tests， liver and brain indices， liver function， lipid indicators， and histopathological changes in the liver and brain tissue. RNA-seq technology was used to conduct transcriptomic analysis of mouse liver tissue， and differentially expressed genes were screened and subjected to Kyoto Encyclopedia of Genes and Genomes （KEGG） analysis. Key genes were further verified by Western blot and Real-time polymerase chain reaction（Real-time PCR）.ResultsBehavioral tests， liver function， lipid indicators， and histopathological changes in the liver and brain tissue all demonstrated that Erchentang had therapeutic effects on depression in obese mice. KEGG pathway enrichment analysis of transcriptomic data indicated that Erchentang treated depression in obese mice mainly through the peroxisome proliferator-activated receptor （PPAR） signaling pathway. Western blot and Real-time PCR results showed that compared with the model group， the low-， medium-， and high-dose Erchentang groups exhibited downregulated expression of fatty acid-binding protein （FABP） 1 （P<0.01） and upregulated expression of acyl-CoA oxidase （ACOX） 1， PPARα， cholesterol 7α-hydroxylase （CYP7A） 1， and phosphoenolpyruvate carboxy kinase （PCK） 1 （P<0.05） in the liver tissue.ConclusionErchentang exerts therapeutic effects on obesity-associated depression by regulating the PPAR signaling pathway and the expression of related genes FABP1， ACOX1， PPARα， CYP7A1， and PCK1.Keywords：peroxisome proliferator-activated receptor （PPAR） signaling pathway;Erchentang;obesity-associated depression;therapeutic mechanism72|21|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Mechanism of Zuogui Wan in Improving Nephrotic Syndrome in Rats Based on Regulating Gut Microbiota Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the protective effects of Zuogui Wan （ZGW） decoction on nephrotic syndrome （NS） through the regulation of gut microbiota.MethodsThirty male Sprague-Dawley （SD） rats were randomly divided into five groups， with 6 rats in each group： The control group， model group， low-dose group， medium-dose group， and high-dose group. The NS rat model was induced by tail vein injection of 6.5 mg·kg-1 doxorubicin. After successful modeling， the control and model groups were gavaged with normal saline （10 mL·kg-1） twice daily， while the low- （50 mg·kg-1）， medium- （100 mg·kg-1）， and high-dose （200 mg·kg-1） groups were gavaged with ZGW （10 mL·kg-1） twice daily. All rats were administered at fixed intervals daily for 8 consecutive weeks. The therapeutic effects of ZGW on NS in rats were observed， and the optimal dose was screened. Renal and intestinal pathological changes in rats were examined. Fecal samples were collected， and 16S rDNA sequencing technology was used to detect the diversity and abundance of gut microbiota in each group.ResultsCompared with the control group， 24-hour urinary protein， serum creatinine， urea nitrogen， and cholesterol levels significantly increased in the model group （P<0.01）， while serum albumin levels decreased （P<0.01）. These changes were ameliorated in the treatment groups （P<0.05， P<0.01）. Renal pathology revealed intact and orderly arranged glomeruli and renal tubules in the control group. In the model group， glomerular atrophy， widened mesangial areas， podocyte swelling， disordered renal tubular arrangement， and numerous casts were observed. Varying degrees of glomerular atrophy and disordered renal tubular arrangement were seen in the treatment groups. Specific protein assays revealed increased serum levels of kidney injury molecule-1（KIM-1） and α1-microglobulin （P<0.01）， and significantly decreased levels of E-cadherin， Podocin， and Nephrin in renal tissues （P<0.01）， along with a significant increase in transforming growth factor-β（TGF-β） （P<0.01） in the model group. In the treatment groups， serum KIM-1 and α1-microglobulin levels decreased， E-cadherin levels significantly increased （P<0.01）， and TGF-β levels significantly decreased （P<0.01）. Podocin and Nephrin levels increased in the high-dose group （P<0.05）. Additionally， intestinal mucosal atrophy， epithelial cell edema， decreased goblet cells， and multiple inflammatory infiltrations were observed in the model group. The sequencing results of gut microbiota demonstrate that ZGW can significantly ameliorate intestinal dysbiosis in rats， restore the abundance of beneficial bacteria， and exert a profound influence on the compositional profile of gut microbiota.ConclusionZGW can alleviate renal injury in rats with nephrotic syndrome by improving gut microbiota and protecting the intestinal barrier.Keywords：Zuogui Wan;nephrotic syndrome;gut microbiota;rats75|20|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Modified Taohe Chengqitang Regulates Notch/eNOS Signaling Pathway to Inhibit Hepatic Sinusoidal Capillarization Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate whether modified Taohe Chengqitang （JTCT） treats liver fibrosis by inhibiting hepatic sinusoidal capillarization， and to verify whether its specific mechanism is related to the Homologous genes responsible for the notches along the edges of Drosophila wings（Notch） signaling pathway and endothelial nitric oxide synthase （eNOS） signaling pathway.MethodsFifty C57BL/6 mice were randomized into 5 groups： Control， model （5 mL·kg-1·3 d-1）， low-dose JTCT， medium-dose JTCT， and high-dose JTCT （JTCT-L，JTCT-M，JTCT-H）. Except the control group， the other groups were intraperitoneally injected with 20% carbon tetrachloride （CCl4） olive oil solution every 3 days for 4 weeks to induce liver fibrosis. Meanwhile， JTCT-L， JTCT-M， and JTCT-H groups were administrated with JTCT by gavage at doses of 16.6， 33.3， and 66.6 g·kg-1·d-1， respectively， for 4 consecutive weeks （the control and model groups received equal volumes of normal saline by gavage）. Primary liver sinusoidal endothelial cells （LSECs） were isolated from rat livers through in situ perfusion of collagenase， Percoll density gradient centrifugation， and selective removal of Kupffer cells. After verification of cell phenotype， LSECs were used for experiments. For cells at the logarithmic growth phase， the small interfering RNA（siRNA） kit was used to knock down the expression of soluble guanylate cyclase （sGC） through transient transfection. Subsequently， the Notch agonist Jagged-1 was applied. Cell counting kit-8 （CCK-8） was used to examine the cytotoxicity of JTCT on LSECs. Real-time PCR and Western blot were employed to measure the expression of molecules in the Notch and eNOS signaling pathways at mRNA and protein levels， respectively. Intracellular Ca2+ was labeled with the fluorescent probe Fluo-4 acetoxymethyl ester（Fluo-4/AM）.ResultsThe animal experiment showed that compared with the control group， the model group exhibited hepatic steatosis， inflammatory cell infiltration， hepatocyte degeneration and necrosis， lobular structural disorder， and fibrous tissue hyperplasia in the mouse liver tissue， significantly elevated serum levels of hydroxyproline （Hyp）， alanine transaminase （ALT）， and aspartate transaminase （AST） （P<0.01）， significantly upregulated expression levels of Notch1， Hes family bHLH transcription factor 1（Hes1）， Cluster of Differentiation 31（CD31）， and von Willebrand factor（vWF） （P<0.01）， and significantly downregulated phosphorylate（p）-eNOS/eNOS ratio and sGC expression （P<0.01）. Compared with the model group， all the JTCT groups showed significantly reduced serum Hyp， ALT， and AST levels （P<0.01）， downregulated expression of Notch1， Hes1， CD31， and vWF （P<0.05， P<0.01）， and upregulated p-eNOS/eNOS ratio and sGC expression （P<0.05， P<0.01） in the liver tissue， with the JTCT-H group showing the most significant changes （P<0.01）. The cell experiment showed that compared with the LSEC-1day group， the LSEC-5day group exhibited significantly increased expression of Notch1， Hes1， CD31， and vWF （P<0.01）， significantly decreased p-eNOS/eNOS ratio and sGC expression （P<0.01）， and elevated intracellular Ca2+ concentration （P<0.01）. Compared with the LSEC-5day group， the JTCT group showed decreased expression of Notch1， Hes1， CD31， and vWF （P<0.01）， significantly increased p-eNOS/eNOS ratio （P<0.01）， and significantly reduced intracellular Ca2+ concentration （P<0.01）. No significant differences were observed in the expression of Notch1， Hes1， eNOS， p-eNOS， CD31， vWF， sGC， or intracellular Ca2+ concentration between the Jagged1 group and the Jagged1+JTCT group. Compared with the LSEC-5day group， the sGC knockout group （sGC-KO） showed significantly increased expression of CD31 and vWF （P<0.01）. There was no significant difference in CD31 or vWF expression between the sGC-KO group and the sGC-KO+JTCT group.ConclusionJTCT inhibits the activation of the Notch signaling pathway and restores the activity of the eNOS signaling pathway to suppress sinusoidal capillarization of LSECs， thereby treating liver fibrosis.Keywords：modified Taohe Chengqitang;hepatic sinusoidal capillarization;Homologous genes responsible for the notches along the edges of Drosophila wings（Notch） signaling pathway;endothelial nitric oxide synthase（eNOS） signaling pathway;liver fibrosis83|18|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03- Abstract：ObjectiveTo observe the effect and therapeutic effect of Kaixuan Jiedu core prescription （KXJD） on skin homing of Th17 cells in the mouse model of imiquimod （IMQ） combined with restraint stress-induced psoriasis-like skin damage， and to explore its potential mechanism from the perspective of neuro-immune axis.MethodsThirty male C57BL/6J mice were randomly allocated into five groups （n=6）： Control， model （IMQ）， restraint stress model （IMQ+RS）， KXJD， and methotrexate （MTX）. The mouse model of psoriasis-like skin damage was established by 5% IMQ combined with restraint stress. At the same time of modeling， each treatment group was treated with corresponding doses of drugs， and the control， IMQ， and IMQ+RS groups were treated with the same amount of normal saline by gavage once a day for 5 days. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in the skin tissue and Baker scoring was performed. Serum levels of interleukin-1β （IL-1β） and angiopoietin-2 （Ang-2） were measured by enzyme-linked immunosorbent assay （ELISA）. The levels of matrix metalloproteinase-9 （MMP-9）， tissue inhibitor of metalloproteinase-1 （TIMP-1）， C-C motif chemokine ligand 20 （CCL20）， and C-C motif chemokine receptor 6 （CCR6） in the skin tissue were determined. Immunohistochemistry （IHC） was employed to determine the protein expression of cutaneous lymphocyte-associated antigen （CLA）， integrin αE （CD103）， cytokeratin 10 （CK10）， and nuclear factor-kappa B （NF-κB） in the skin. Immunofluorescence double staining （DIF） was adopted to detect the expression and co-localization of vascular endothelial cadherin （VE-cadherin） and platelet-endothelial cell adhesion molecule （CD31）， CCR6， CD103， substance P （SP）， calcitonin gene-related peptide （CGRP）， and protein gene product 9.5 （PGP9.5） in the skin tissue. Real-time PCR was employed to quantify the mRNA levels of IL-10， IL-17A， and IL-23.ResultsCompared with the control group， the IMQ group and IMQ+RS group showed significant inflammatory cell infiltration， abnormal proliferation of epidermal cells， keratinization and other pathological changes in the skin tissue， and a significant increase in Baker score， elevated levels of IL-1β and Ang-2 in the serum and MMP-9， CCL20 and CCR6 in the skin lesions， upregulated expression of CLA， CD103， CK10， NF-κB， IL-17A mRNA， and IL-23 mRNA in the skin lesions， and downregulated expression of TIMP-1 and IL-10 mRNA. In addition， the fluorescence intensities of VE-cadherin and CD31 co-localization， CCR6 and CD103 co-localization， SP and PGP9.5 co-localization， and CGRP and PGP9.5 co-localization were increased （P<0.05）. Compared with the IMQ group， the above indicators in the IMQ+RS group were further aggravated. Compared with the IMQ group， the above indicators in the IMQ+RS group were further aggravated. Compared with the IMQ+RS group， KXJD and MTX significantly alleviated the pathological damage of skin lesions， significantly decreased the Baker score， lowered the levels of IL-1β and Ang-2 in the serum and MMP-9， CCL20 and CCR6 in skin lesions， downregulated the expression of CLA， CD103， CK10， NF-κB， IL-17A mRNA and IL-23 mRNA in skin lesions， and upregulated the expression of TIMP-1 and IL-10 mRNA. Furthermore， KXJD and MTX reduced the fluorescence intensities of VE-cadherin and CD31 co-localization， CCR6 and CD103 co-localization， CGRP and PGP9.5 co-localization， and SP and PGP9.5 co-localization （P<0.05）.ConclusionKXJD can significantly ameliorate the psoriasis-like skin damage induced by IMQ combined with restraint stress in mice by regulating the neural-immune axis and inhibiting the skin homing of Th17 cells.Keywords：psoriasis;Kaixuan Jiedu prescription （KXJD）;restraint stress;immunity;neuroinflammation;Th17 cells;homing;mice57|15|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
- Abstract：ObjectiveTo establish the mouse models of psoriasis-like lesions induced by continuous cold exposure or intermittent cold exposure combined with imiquimod （IMQ）， and to evaluate the interventional effects of Kaixuan Jiedu core prescription （KXJD） on the two models.MethodsMale C57BL/6J mice were selected and classified into two experimental batches. The first batch of 36 mice was randomized into a room temperature group， a continuous cold exposure （10 ℃/24 h） group， and an intermittent cold exposure （10 ℃/6 h） group. Each group was further divided into a normal subgroup and a model subgroup （topical application of IMQ to induce skin lesions）， with 6 mice in each subgroup， for modeling and evaluation. The second batch of 54 mice， with 6 in each group， were subjected to the same temperature grouping with an additional KXJD （30.42 g·kg-1， continuous gavage for 5 days） group. Comprehensive evaluation of model characteristics and KXJD efficacy was conducted through Psoriasis Area and Severity Index （PASI） scoring， skin temperature measurement by infrared thermography， histopathological observation by hematoxylin-eosin （HE） staining， detection of vascular endothelial growth factor （VEGF） and platelet endothelial cell adhesion molecule 1 （CD31） by immunohistochemistry， detection of Claudin-1 and Occludin by immunofluorescence assay， determination of serum levels of tumor necrosis factor-α （TNF-α） and interleukin （IL）-10 by enzyme-linked immunosorbent assay （ELISA）， and quantification of mRNA levels of IL-17A， IL-23， IL-6， and chemokine ligand 20 （CCL20） in skin lesions by quantitative Real-time polymerase chain reaction （Real-time PCR）.ResultsModel mice in all temperature groups exhibited typical psoriasis-like skin lesions. Compared with the normal groups， the model groups showed increased PASI scores， decreased skin temperatures （P<0.05）， obvious epidermal thickening， parakeratosis， and dermal inflammatory cell infiltration， as well as elevated mRNA levels of IL-17A， IL-23， IL-6， and CCL20 （P<0.05）. Cold exposure further aggravated psoriasis. The total PASI score of the intermittent cold exposure model group was higher than that of the room temperature model group （P<0.05）. The serum IL-10 did not show a compensatory elevation， and the blood vessels presented a characteristic of elevated CD31 expression （P<0.05） without a synchronous increase in VEGF. The continuous cold exposure model group exhibited more significant dermal capillary tortuosity and dilation， with the highest mRNA levels of IL-17A， IL-23， IL-6， and CCL20 among all groups. Compared with the respective model groups， KXJD intervention alleviated skin lesions， reduced epidermal thickness and inflammatory cell infiltration， and increased skin temperature， with the temperature increase being particularly significant in the intermittent cold exposure+KXJD group （P<0.05）. Furthermore， KXJD down-regulated the expression of VEGF and CD31， restored the expression of Claudin-1 and Occludin， decreased the mRNA levels of IL-17A and IL-23 （P<0.05）， and reduced the serum TNF-α level.ConclusionThis study successfully established compound psoriasis-like mouse models induced by cold exposure combined with IMQ. It confirms that cold aggravates the severity of psoriasis by exacerbating the closure of Xuanfu （sweat pores）， microcirculation disorders， and immune imbalance. Moreover， different cold exposure patterns have distinct mechanism differences. Continuous cold exposure focuses on enhancing the inflammatory response via the IL-23/IL-17 axis and angiogenesis， simulating chronic aggravation under a long-term cold environment. Intermittent cold exposure tends to impair immune regulation and induce microvascular endothelial stress， corresponding to acute exacerbations caused by sudden temperature drops. KXJD can effectively alleviate psoriasis-like skin lesions under cold conditions by unblocking Xuanfu， regulating vasomotor function， and correcting abnormal immune-inflammatory responses.Keywords：cold exposure;temperature variation;psoriasis;Kaixuan Jiedu core prescription;model construction74|16|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
Kaixuan Jiedu Core Prescription Alleviates Restraint Stress-exacerbated Imiquimod-induced Psoriasis-like Skin Lesions via Regulation of HPA Axis and Neuroinflammation Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the ameliorative effect and potential mechanisms of Kaixuan Jiedu core prescription （KXJD） on imiquimod （IMQ）-combined restraint stress-induced psoriasis-like skin lesions in mice.MethodsA total of 36 C57BL/6J mice were randomly assigned to six groups （n=6 per group）： Normal group， restraint stress blank group， model group， restraint stress model group， KXJD group （30.42 g·kg-1）， and methotrexate group （0.001 g·kg-1）. Psoriasis-like lesions were induced by topical IMQ application combined with restraint stress. After 5 days of intervention， the severity of skin lesions was evaluated using the Psoriasis Area and Severity Index （PASI）. The following parameters were assessed： Hypothalamic-pituitary-adrenal （HPA） axis-related hormones， including adrenocorticotropic hormone （ACTH）， corticotropin-releasing hormone （CRH）， and corticosterone （CORT）， central neuronal markers， including neuronal nuclei antigen （NeuN）， microtubule-associated protein 2 （MAP2）， and beta Ⅲ-tubulin （β-Ⅲ tubulin）， microglial activation markers， including ionized calcium-binding adapter molecule-1 （Iba-1） and cluster of differentiation 11b （CD11b）， and skin nerve fiber markers， including protein gene product 9.5 （PGP9.5） and serotonin （5-HT）， as well as the expression levels of inflammatory cytokines tumor necrosis factor-alpha （TNF-α）， interleukin-6 （IL-6）， and interleukin-1 beta （IL-1β）.ResultsCompared with the normal group， both the model group and the restraint stress model group exhibited more severe psoriasis-like skin lesions， with significantly elevated serum levels of ACTH， CRH， and CORT （P<0.01）. The expression of glucocorticoid receptor （GR） and corticotropin-releasing hormone receptor 1 （CRHR1） in the skin was significantly downregulated. The expression of NeuN， MAP2， β-Ⅲ tubulin， Iba-1， and CD11b in the hypothalamus and hippocampus was significantly upregulated， suggesting abnormal changes in neuronal number or structure and aberrant activation of glial cells （P<0.05， P<0.01）. In addition， the expression of PGP9.5 and 5-HT in the skin， as well as the mRNA levels of TNF-α， IL-6， and IL-1β were all markedly elevated （P<0.05， P<0.01）. Compared with the model group， the restraint stress model group showed further exacerbation in most parameters. Compared with the restraint stress model group， the KXJD group exhibited significantly reduced PASI scores （P<0.01）， significantly decreased serum CRH， ACTH， and CORT levels （P<0.05， P<0.01）， upregulated skin GR and CRHR1 expression， inhibited abnormal neuronal changes and microglial activation in the hypothalamus and hippocampus， attenuated skin nerve fiber hyperplasia and amine signaling molecule release， and significantly reduced pro-inflammatory cytokine mRNA expression （P<0.05， P<0.01）.ConclusionKaixuan Jiedu Core prescription can effectively ameliorate IMQ combined with restraint stress-induced psoriasis-like skin lesions in mice by modulating HPA axis function， inhibiting central neuropathological changes， and attenuating skin nerve fiber hyperplasia， amine signaling molecule （5‑HT） release and local inflammatory responses.Keywords：Kaixuan Jiedu core prescription （KXJD）;psoriasis;restraint stress;hypothalamic-pituitary-adrenal axis;inflammation15|4|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Kaixuan Jiedu Core Prescription Alleviates Psoriatic Skin Lesions in Mice by Modulating Cold-sensitive TRPM8 Neuron-derived Signaling Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the ameliorative effects of Kaixuan Jiedu core prescription （KXJD） on skin lesions in psoriasis-like mouse models under cold environment exposure， and to analyze its influences on transient receptor potential （TRP） channels and related neuroimmune regulatory factors.MethodsThirty-six C57BL/6J mice were randomized into 6 groups， with 6 mice in each group. Two feeding conditions were set： Normal temperature and cold ［simulating a cold environment at （10±0.5） ℃， for 6 h daily］. Mice were induced to develop psoriasis-like lesions by applying imiquimod externally. The model mice were allocated into model groups and KXJD （30.42 g·kg-1， continuous gavage for 5 days） groups. Normal mice were used as the control group. Specifically， mice were allocated into normal temperature， normal temperature model， normal temperature+KXJD， cold exposure control， cold exposure model， and cold exposure+KXJD groups. The pathological changes in skin lesions were observed by hematoxylin-eosin （HE） staining. The expression of cluster of differentiation （CD） 3+ T lymphocytes， CD11c+ dendritic cells （DCs）， phosphorylated extracellular signal-regulated kinase （p-ERK）， and substance P （SP） were detected by immunofluorescence assay. The protein level of transient receptor potential cation channel subfamily M member 8 （TRPM8） in the skin tissue was determined by Western blot. The expression of TRPM8， transient receptor potential cation channel subfamily V member 1 （TRPV1）， transient receptor potential cation channel subfamily A member 1 （TRPA1）， and transient receptor potential cation channel subfamily V member 2 （TRPV2） at the protein and mRNA levels was determined by immunohistochemistry and Real-time PCR， respectively. The levels of calcitonin gene-related peptide （CGRP） and neuropeptide Y （NPY） in the serum were analyzed by enzyme-linked immunosorbent assay （ELISA）. The enrichment analysis of differentially expressed genes （DEGs） and TRP pathway network construction were conducted based on the GEO database. The co-expression of TRPM8 and CGRP in the skin lesions was verified by immunofluorescence double labeling.ResultsBoth the normal temperature and cold exposure model groups showed typical psoriasis-like skin lesions. Compared with the normal temperature and cold exposure control groups， the model groups had excessive epidermal keratinization， thickened spinous layer， and inflammatory infiltration in the dermis， with increased pathological scores （P<0.05）， increased infiltration of CD3+ and CD11c+ cells and expression of p-ERK and SP， upregulated mRNA levels of TRPM8， TRPA1， and TRPV2， downregulated mRNA level of TRPV1 （P<0.05）， and reduced content of CGRP and increased content of NPY in the serum. Compared with the normal temperature and cold exposure model groups， KXJD reduced the pathological manifestations and pathological scores of psoriasis-like skin lesions （P<0.05）， and inhibited the infiltration of CD3+ and CD11c+ cells and the expression of p-ERK and SP. Gene enrichment analysis suggested that the DEGs of psoriasis were significantly enriched in the interleukin （IL）-17 signaling pathway and TRP channel inflammatory regulation. Compared with the normal temperature and cold exposure model groups， KXJD reversed the abnormal mRNA levels of genes related to the TRP channel subfamilies （P<0.05）， increased the CGRP level， and decreased the NPY level. Immunofluorescence double labeling further confirmed that compared with the model groups， KXJD down-regulated the co-expression of TRPM8 and CGRP in the skin lesions.ConclusionKXJD may ameliorate psoriasis-like skin lesions by downregulating the overexpressed cold-sensitive receptor TRPM8 in skin lesions and correcting the disorder of neuropeptide （such as SP and CGRP） release mediated by it， thereby inhibiting the IL-23/helper T cell 17 （Th17） core inflammatory pathway， suppressing the infiltration of inflammatory cells and the activation of the ERK signaling pathway， and regulating the Xuanfu （sweat pore）-TRPM8-neuroimmune response axis.Keywords：Kaixuan Jiedu core prescription;psoriasis;transient receptor potential cation channel subfamily M member 8 （TRPM8）;neuroimmunology;Xuanfu （sweat pore）105|19|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Mechanism of Kaixuan Jiedu Core Prescription in Ameliorating Psoriasis-like Inflammation via TrkA Receptor-mediated Regulation of CGRP Expression and Dendritic Cell Activation Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the ameliorative effects and mechanisms of Kaixuan Jiedu core prescription （KXJD） on neuroimmunological inflammation in imiquimod （IMQ）-induced psoriasis-like mice.MethodsA total of 24 C57BL/6J mice were randomly divided into four groups （n=6）： Normal， model， KXJD， and tropomyosin receptor kinase A （TrkA） inhibitor GW441756 groups. The mice in the model， KXJD， and GW441756 groups were topically treated with 5% IMQ cream （62.5 mg·d-1） on the back to induce psoriasis-like inflammation. The KXJD group received KXJD by gavage （30.42 g·kg-1）， the GW441756 group received intraperitoneal injection of GW441756 （10 mg·kg-1）， and the normal and model groups received an equal volume of normal saline by gavage， with continuous intervention for 5 days. The severity of skin lesions was evaluated using the psoriasis area and severity index （PASI）. Hematoxylin-eosin （HE） staining was used to measure epidermal thickness and observe pathological changes in the lesioned skin. Immunohistochemistry was employed to detect the expression of proliferating cell nuclear antigen （Ki67） and interleukin-17A （IL-17A） in the lesioned skin. Enzyme-linked immunosorbent assay （ELISA） was used to quantify the levels of interleukin-23 （IL-23） and calcitonin gene-related peptide （CGRP） in the lesioned tissues. Western blot was used to detect the expression of TrkA and phosphorylated TrkA （p-TrkA）. Immunofluorescence assay was performed to detect the expression of TrkA receptor， protein gene product 9.5 （PGP9.5）， cluster of differentiation 11c （CD11c）， and CGRP in the lesions. Flow cytometry was used to detect the activation of splenic dendritic cells （DCs）.ResultsCompared with the normal group， the model group exhibited typical psoriasis-like inflammation， characterized by erythema， infiltration and scaling， with histopathological findings of epidermal hyperkeratosis and acanthosis. The model group showed significantly increased expression of Ki67， IL-17A， IL-23 and p-TrkA （P<0.05， P<0.01）， increased fluorescence intensity of CD11c， and significantly decreased CGRP expression （P<0.05）. The splenic DC activation was significantly enhanced， as indicated by the increased mean fluorescence intensity （MFI） of CD86 （P<0.05）. Compared with the model group， both the KXJD and GW441756 groups showed amelioration of the psoriasis-like skin inflammation， with significantly down-regulated expression of IL-17A， IL-23 and p-TrkA （P<0.05， P<0.01）， significantly up-regulated expression of CGRP （P<0.01）， reduced CD11c+ DC infiltration， and restored splenic DC activation balance （down-regulated CD86 MFI and up-regulated CD80 and CD40 MFI）. Furthermore， the inhibitory effect of KXJD on Ki67 was significantly superior to that of the GW441756 group （P<0.01）.ConclusionKXJD may alleviate IMQ-induced psoriasis-like inflammation in mice by targeting and inhibiting TrkA receptor phosphorylation， regulating CGRP expression in the lesions， and ameliorating aberrant activation of dendritic cells， while also significantly inhibiting keratinocyte proliferation.Keywords：Kaixuan Jiedu core prescription;psoriasis;calcitonin gene-related peptide （CGRP）;tropomyosin receptor kinase A （TrkA） receptor;neuroimmunological inflammation;dendritic cells17|2|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Kaixuan Jiedu Core Prescription Ameliorates Imiquimod-induced Psoriasis-like Skin Lesions in Mice by Inhibiting Neuroinflammation Mediated by NGF-TrkA/TRPV1-PAR-2 Signaling Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the effects and molecular mechanisms of Kaixuan Jiedu core prescription （KXJD） on neuroinflammation and immuno-inflammation in the mouse model of imiquimod （IMQ）-induced psoriasis-like skin lesions by regulating the nerve growth factor （NGF）-tropomyosin receptor kinase A （TrkA）/transient receptor potential vanilloid 1 （TRPV1）-protease-activated receptor-2 （PAR-2） signaling pathway.MethodsA psoriasis-like skin lesion model was established in male C57BL/6J mice with IMQ. A total of 24 mice were randomized into four groups （n=6 per group）： Blank control， model， methotrexate （MTX， 1 mg·kg-1）， and KXJD （30.42 g·kg-1）. Immunohistochemistry was employed to detect the expression of cluster of differentiation 3 （CD3）， EGF-like module-containing mucin-like hormone receptor-like 1 （F4/80）， lymphocyte antigen 6 complex locus G （Ly-6G）， substance P （SP）， calcitonin gene-related peptide （CGRP）， NGF， phosphorylated TrkA （p-TrkA）， phosphorylated TRPV1 （p-TRPV1）， and PAR-2 in skin lesions. Serum levels of interleukin-17A （IL-17A） and interleukin-23 （IL-23） were measured by enzyme-linked immunosorbent assay （ELISA）. Immunofluorescence assay and Western blot were employed to determine the expression of phosphorylated p38 mitogen-activated protein kinase （p-p38 MAPK） and phosphorylated nuclear factor-κB p65 （p-NF-κB p65）. Reverse transcription quantitative polymerase chain reaction （Real-time PCR） was used to measure the mRNA levels of interleukin-1β （IL-1β）， tumor necrosis factor （TNF）， interleukin-6 （IL-6）， and C-X-C motif chemokine ligand 1 （CXCL1） in skin lesions. Correlation analysis was performed.ResultsCompared with the blank control group， the model group showed increased positive areas of CD3+， F4/80+， and Ly-6G+ in skin lesions （P<0.05）， elevated serum levels of IL-17A and IL-23 （P<0.05）， increased positive areas of SP and CGRP in skin lesions （P<0.05）， increased positive areas of NGF， p-TrkA， p-TRPV1， and PAR-2 （P<0.05）， elevated ratios of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 （P<0.05）， and upregulated mRNA levels of IL-1β， TNF， IL-6， and CXCL1 （P<0.05）. Compared with those in the model group， all the above indicators were reversed in the KXJD group （P<0.05）. MTX only downregulated the expression of p-TRPV1 and PAR-2 （P<0.05）， with no significant effects on the expression of NGF， p-TrkA， or CGRP.ConclusionKXJD inhibits the NGF-TrkA/TRPV1-PAR-2 signaling pathway to reduce neuropeptide release and simultaneously downregulates the p38 MAPK/NF-κB signaling pathway and the expression of downstream pro-inflammatory factors to ameliorate psoriasis-like neuroinflammation and immuno-inflammation. The therapeutic effect of KXJD on psoriasis-like inflammation is closely associated with the inhibition of the NGF-TrkA/TRPV1-PAR-2 signaling pathway. This study provides experimental evidence for the modern interpretation of the Xuanfu theory.Keywords：Kaixuan Jiedu core prescription;psoriasis;neuroinflammation;nerve growth factor-tropomyosin receptor kinase A/transient receptor potential vanilloid 1-protease-activated receptor-2 （NGF-TrkA/TRPV1-PAR-2） signaling pathway;p38 mitogen-activated protein kinase （p38 MAPK）/nuclear factor-κB （NF-κB） signaling pathway68|15|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03- Abstract：Gastric precancerous lesions， often presenting as decreased appetite， weight loss， fatigue， epigastric fullness， and upper abdominal pain， pose challenges to treatment and considerably affect patients' quality of life. Pathologically， these lesions are characterized by alterations in the gastric mucosa accompanied by intestinal metaplasia or dysplasia， which markedly elevate the risk of developing gastric cancer. Traditional Chinese medicine （TCM） practitioners have explored various therapeutic approaches focusing on invigorating the spleen， resolving dampness， clearing heat， addressing phlegm accumulation， activating blood， and detoxifying. For contemporary populations suffering from gastric precancerous lesions， our team has innovatively proposed a core pathogenesis theory encompassing deficiency， stagnation， phlegm， stasis， and toxin. Furthermore， our team has developed a comprehensive prevention and treatment framework： Invigorating the spleen and harmonizing the stomach （foundational principles）， balancing and restoring Qi movement （primary objectives）， resolving phlegm and unblocking collaterals （routine practices）， detoxifying and dissipating nodules （critical interventions）， and comprehensive health management （supportive care）. This framework provides a robust theoretical foundation along with practical guidance for preventing and treating diseases related to the spleen-stomach axis. From a pathological perspective， key interventions for managing gastric precancerous lesions include restoring integrity of the gastric mucosae while regulating its microenvironmental conditions and enhancing mucosal circulation， which are integral throughout the entire treatment process. On this basis， a full-course chain of prevention and treatment has been established within clinical practice， encompassing functional gastrointestinal disorders-superficial gastritis-atrophic gastritis-gastric precancerous lesions-prevention and treatment post-endoscopic submucosal dissection. The guiding principles of this treatment approach involve invigorating the spleen， regulating Qi movement， resolving phlegm， unblocking collaterals， and detoxifying. TCM compound formulas such as Jianpi Tongluo Jiedu prescription and Hezhong Xiaopi granules， as well as Chinese patent medicines like Weifuchun and Moluodan， can be used for treating gastric precancerous lesions at different stages. Through medicinal regulation， the state of the gastric mucosa can be improved， and thus the development of gastric precancerous lesions can be curbed from the perspective of full-course prevention and treatment.Keywords：core pathogenesis of deficiency， stagnation， phlegm， stasis， and toxin;full-course prevention and treatment;gastric precancerous lesions;chronic atrophic gastritis;innovative theory;clinical application8|2|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
Hezhong Xiaopi Granules Regulate Ncln-CHOP Axis to Inhibit Endoplasmic Reticulum Stress and Reduce Gastric Mucosal Cell Apoptosis Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the effect of Hezhongxiaopi granules （HZXPG） on methylnitronitrosoguanidine （MNNG）-mediated gastric mucosal cell apoptosis and the regulatory effects on the Nicalin （Ncln）-C/EBP homologous protein （CHOP） axis and endoplasmic reticulum stress （ERS）.MethodsThe cell counting kit-8 （CCK-8） assay was employed to examine the inhibitory effect of MNNG on the proliferation of GES-1 cells， and the optimal effective dose of MNNG was selected. Human gastric mucosal GES-1 cells were allocated into the control， model （MNNG， 1.562 5 mmol·L-1）， and low/high-dose HZXPG （5% and 10% HZXPG-containing serum） groups. Phalloidin staining was employed to detect MNNG-induced morphological changes in human gastric mucosal cells. Terminal deoxynucleotidyl transferase dUTP nick end labeling （TUNEL） assay was adopted to assess cell apoptosis. Annexin Ⅴ/propidium iodide （Annexin Ⅴ/PI） flow cytometry was utilized to measure the alterations in the apoptotic cycle of human gastric mucosal cells. Western blot was performed to determine the expression levels of proteins related to apoptosis， ERS， and the Ncln/CHOP axis.ResultsCompared with the control group， the model group exhibited a reduction in the surface area of GES-1 cells， endoplasmic reticulum （ER） dilation， increased early and late apoptosis rates of gastric mucosal cells， upregulated protein levels of truncated Bid （tBid）， Bcl-2-associated X protein （Bax）， cleaved-cysteinyl aspartate-specific proteinase （Caspase）-3， and cleaved-Caspase-8， and downregulated protein level of B-cell lymphoma-2 （Bcl-2） （P<0.01）. In addition， the expression levels of binding immunoglobulin protein （BiP）， Ncln， and CHOP were upregulated （P<0.01）， with enhanced Ncln expression in the ER and elevated CHOP expression in the nucleus. Compared with the model group， the high-dose HZXPG group showed a significant increase in the surface area of gastric mucosal cells. Both dose groups exhibited inhibited ER dilation and reduced early and late apoptosis rates of gastric mucosal cells （P<0.01）. Low-dose HZXPG decreased the expression of tBid and Bax （P<0.05， P<0.01） and promoted Bcl-2 expression （P<0.01）. High-dose HZXPG reduced the expression levels of tBid， Bax， cleaved-Caspase-3， and cleaved-Caspase-8 （P<0.05， P<0.01） and increased the Bcl-2 expression level （P<0.05）. Furthermore， high-dose HZXPG downregulated the expression levels of BiP， Ncln， and CHOP （P<0.05， P<0.01）， while decreasing the nuclear translocation of CHOP.ConclusionHZXPG alleviates MNNG-induced ERR-mediated apoptosis of gastric mucosal cells by inhibiting the Ncln-CHOP axis， thereby relieving gastric mucosal cell damage caused by precancerous gastric lesions.Keywords：Hezhongxiaopi granules;chronic atrophic gastritis;gastric precancerous lesion;endoplasmic reticulum stress;apoptosis;Nicalin （Ncln）-C/EBP homologous protein （CHOP） axis7|2|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Theoretical and Practical Analyses of Traditional Chinese Medicine in Prevention and Treatment of Senile Chronic Atrophic Gastritis AI Introduction
Abstract：Senile chronic atrophic gastritis （SCAG） is a condition characterized by high prevalence， prolonged duration， and difficulty in treatment， along with a significant risk of carcinogenesis. This severely impacts the quality of life among the elderly population in China. The prevention and management of SCAG represent one of the most urgent and prominent needs within the current health care and elderly care sectors. However， existing treatment options are limited， with insufficient mucosal repair following Helicobacter pylori eradication， as well as a lack of effective methods to reverse atrophy or intestinal metaplasia. The primary objectives in treating chronic gastritis in older adults are symptom relief and alleviation of mucosal histological abnormalities. Traditional Chinese medicine （TCM） offers unique advantages for managing patients with SCAG. Therefore， utilizing TCM methodologies underpinned by TCM theory to prevent and treat the progression of SCAG holds considerable clinical significance. Our research team has been dedicated to theoretical， clinical， and fundamental investigations into gastric precancerous lesions and SCAG for an extended period. This article systematically reviews the intricate causal relationship between the spleen-stomach system and aging while elucidating TCM pathogenesis of SCAG as internal deficiency coupled with excess in manifestations. It explores evolutionary patterns of dampness， stagnation， stasis， toxicity， and deficiency and proposes a progressive pathogenic evolution chain： Aging-deficiency of spleen and kidney-imbalance of Qi and blood-phlegm turbidity accompanied by Qi stagnation-accumulation of phlegm， stasis， and toxicity-weakness of stomach collaterals. The core treatment principle emphasizes simultaneous treatment targeting both spleen and kidney as its foundation while employing strategies such as promoting Qi movement to resolve dampness， alongside efforts aimed at removing stasis and detoxifying as primary approaches. Finally， this article summarizes current research achievements in TCM interventions for SCAG， aiming to provide new insights for clinical practice and scientific research in TCM interventions for SCAG.Keywords：senile chronic atrophic gastritis;pathogenesis evolution patterns;pathogenesis evolution chain;simultaneous treatment of spleen and kidney9|3|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03- Abstract：Ulcerative colitis （UC）， a chronic nonspecific inflammatory bowel disease characterized by unclear etiology， complex contributing factors， and a refractory course with malignant transformation potential， imposes a substantial burden on both individual patients and healthcare systems. There is an urgent need to explore effective therapeutic strategies and pharmacological interventions. Professor LIU Zhen， based on years of clinical practice， proposed a dynamic pathogenesis chain of UC： Spleen deficiency with dampness excess as the foundation， dampness obstruction as the nexus， stasis-toxin interaction as the key， and stasis-toxin damaging intestinal collaterals as the terminal outcome. The treatment， following the progression of deficiency （depression）-dampness-toxin-stasis （toxin）， should focus on invigorating the spleen and resolving dampness. A stage-specific treatment approach is emphasized. During the susceptible stage， prevention is recommended， which relies on regulating the diet， maintaining a positive mental state， and adjusting daily routines to invigorate the spleen and replenish Qi. During the acute attack and remission stages， the treatment should be tailored according to clinical typing and disease severity， flexibly employing therapeutic strategies such as tonifying deficiency， resolving depression， eliminating dampness， clearing heat， detoxifying， arresting bleeding， and resolving stasis in order to interrupt disease progression. In the recovery stage， latent pathogenic factors should be addressed while the postnatal constitutional foundation be preserved to prevent recurrence. According to the TCM principle of treating disease before its onset， a whole-course management path of early protection-interception-stratified care-consolidation has been developed， covering all stages of UC， to inform its clinical prevention and treatment.Keywords：ulcerative colitis;spleen deficiency with dampness excess;stasis-toxin damaging collaterals;dynamic pathogenesis cascade;whole-course management7|2|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
- Abstract：ObjectiveTo investigate the mechanism underlying the effects of three formulas of the method of warming Yang and relieving depression on anxiety- and depression-like behaviors in the mice subjected to a two-hit paradigm of maternal separation （MS） combined with restraint stress （RS）.MethodsNeonatal mice were randomly assigned into the following groups： Blank control， MS alone， model （MS+RS）， warming Yang （WY，5.85 g·kg-1）， relieving depression （RD，12.03 g·kg-1）， warming Yang and relieving depression （WYRD，16.71 g·kg-1）， and fluoxetine groups （2.6 mg·kg-1）. MS was conducted on postnatal day 5 （PD5）. Weaning and preventive drug administration were carried out on PD21， and restraint stress was applied on PD90. Anxiety- and depression-like behaviors were assessed using the open field test （OFT）， the elevated zero maze test and tail suspension test （TST）. High-performance liquid chromatography with electrochemical detection （HPLC-ECD） was employed to measure the levels of neurotransmitters， including 5-hydroxytryptamine （5-HT） and dopamine （DA）， in the hippocampus. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression levels of 5-HT1A receptor （5-HT1AR）， serotonin transporter （SERT）， monoamine oxidase A （MAOA）， glucocorticoid receptor （GR）， adrenocorticotropic hormone （ACTH）， corticotropin-releasing hormone （CRH）， brain-derived neurotrophic factor （BDNF）， and tyrosine kinase receptor B （TrkB）. Immunohistochemistry （IHC） was applied to assess the protein expression levels of 5-HT1AR， 5-HT2A receptor （5-HT2AR）， 5-HT2C receptor （5-HT2CR）， GR， and CRH receptor 1 （CRHR1）. The protein expression levels of BDNF and TrkB in the hippocampus were measured using the fully automated protein expression analysis system （Simple Wes）.ResultsIn the behavioral tests， compared with the blank control group， the model group exhibited significant increases in locomotor distance and central area crossings （P<0.05， P<0.01）in OFT， as well as a significant increase in immobility time in the TST （P<0.05）. Compared with the model group， the RD， WYRD， and fluoxetine groups all showed significantly reduced central area crossings （P<0.05， P<0.01）. Regarding neurotransmitter levels， compared with the blank control group， the model group had significantly decreased hippocampal epinephrine （E） and dopamine （DA） content （P<0.05， P<0.01）. Compared with the MS group， the model group showed significant decreases in hippocampal norepinephrine （NE）， E， and 5-HT content （P<0.05， P<0.01）. Compared with the model group， the WY group decreased hippocampal NE， DA， and 5-HT content （P<0.01）， while the RD， WYRD， and fluoxetine groups exhibited significantly increased hippocampal E content （P<0.01）. At the molecular level， compared with the blank control and MS groups， the model group showed significant increases in mRNA levels of 5-HT1AR， SERT， MAOA， ACTH， and CRH （P<0.01）， and significant decreases in mRNA levels of tryptophan hydroxylase （TPH）， GR， BDNF， and TrkB （P<0.01）. Protein expression of 5-HT1AR， 5-HT2AR， and 5-HT2CR was also significantly elevated （P<0.05， P<0.01） in the model group. Compared with the model group， the RD group showed significant decreases in SERT， MAOA， and CRH mRNA （P<0.05， P<0.01）， significant increases in TPH， BDNF， and TrkB mRNA （P<0.01）， significantly reduced protein expression of 5-HT1AR， 5-HT2AR， and 5-HT2CR （P<0.05）， and significantly increased GR protein expression. The WY group showed a significant increase in ACTH mRNA expression （P<0.01）. The fluoxetine group exhibited significant decreases in MAOA and CRH mRNA （P<0.05， P<0.01）， significant increases in TPH， BDNF， and TrkB mRNA （P<0.01）， significantly reduced 5-HT2AR protein expression （P<0.01）， and significantly increased GR protein expression（P<0.05）.ConclusionThe method of warming Yang and relieving depression can ameliorate anxiety- and depression-like behaviors in two-hit mice. Its mechanism may be associated with the BDNF/TrkB signaling pathway， as well as the HPA axis and serotonergic system.Keywords：warming Yang and relieving depression;two-hit;anxiety- and depression-like behaviors;brain-derived neurotrophic factor （BDNF）/tyrosine kinase receptor B （TrkB） signaling pathway;mice14|6|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
Molecular Mechanism Analysis of Dengzhan Shengmai Capsules Against Myocardial Fibrosis After Myocardial Infarction Based on Network Robustness Algorithm Enhanced Publication AI Introduction
Abstract：ObjectiveTo investigate the potential therapeutic effects of Dengzhan Shengmai capsules （DZSM） on myocardial fibrosis after myocardial infarction and decipher the underlying molecular mechanisms by virtue of network robustness algorithm.MethodsA rat model of myocardial infarction was established by ligating the left anterior descending coronary artery. Successfully modeled Sprague-Dawley rats were randomly allocated into a model group， an enalapril group（3.15 mg·kg-1）， and high- and low-dose DZSM groups（226.8，113.4 mg·kg-1）. In addition， a sham group was set up. After four consecutive weeks of intervention， the cardiac function was assessed via echocardiography， and myocardial collagen deposition was observed through Sirius red staining. The key regulatory pathways of DZSM were analyzed by the network robustness algorithm. Enzyme-linked immunosorbent assay （ELISA） and immunofluorescence assay were employed to validate the mechanisms.ResultsCompared with the sham group， the model group exhibited decreased left ventricular ejection fraction （LVEF%） and fractional shortening （FS%） （P<0.01） and increased myocardial collagen volume fraction （CVF%） （P<0.01）. Compared with the model group， high-dose DZSM and enalapril improved LVEF% and FS% （P<0.01）. Both high- and low-dose DZSM reduced the CVF% （P<0.05， P<0.05，）. Network analysis indicated that DZSM exerted its effects by regulating neutrophil infiltration and related inflammatory pathways. Experimental validation showed that DZSM significantly reduced the protein levels of nuclear factor （NF）-κB， Janus kinase 2 （JAK2）， and signal transduction activator and transducer 3 （STAT3） in the cardiac tissue， as well as the levels of chemokine （C-X-C motif） ligand 1 （CXCL1）， interleukin （IL）-1β， neutrophil elastase-DNA complex （NE-DNA）， and myeloperoxidase-DNA complex （MPO-DNA） in the plasma.ConclusionDZSM may ameliorate myocardial fibrosis by inhibiting neutrophil infiltration and extracellular trap formation and regulating the NF-κB/JAK2/STAT3 signaling pathway.Keywords：myocardial infarction;Dengzhan Shengmai capsules;myocardial fibrosis;network robustness;neutrophil15|6|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03- Abstract：ObjectiveTo explore the mechanism by which Qifu Lizhong decoction restores intestinal mucosal barrier function in ulcerative colitis （UC） by regulating the myosin light chain kinase （MLCK）/phosphorylated myosin light chain （p-MLC） signaling pathway.MethodsA rat model of UC with spleen-kidney Yang deficiency syndrome and an in vitro intestinal barrier injury model were established. In vivo experiments were conducted to evaluate the body weight， disease activity index （DAI） scores， and changes in colonic pathological morphology in each group of rats. Enzyme-linked immunosorbent assay （ELISA） was used to measure the levels of tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and myeloperoxidase （MPO）. Transmission electron microscopy （TEM） was employed to observe the morphology and structure of tight junctions （TJ） in rat colonic epithelium. In vitro experiments were conducted to observe the morphology of F-actin in human colon adenocarcinoma cell line-2（Caco-2） cells by phalloidin staining. Combining both in vivo and in vitro approaches， immunohistochemistry （IHC）， immunofluorescence （IF）， and Western blot were applied to detect the expression and phosphorylation levels of TJ proteins ［zonula occludens-1 （ZO-1）， Occludin， Claudin-1］ as well as key proteins in the MLCK/p-MLC signaling pathway.ResultsIn vivo experiments demonstrated that， compared with the normal group， the model group exhibited significant body weight loss， elevated DAI scores and histopathological scores （P<0.01）， increased colonic TNF-α， IL-1β， and MPO levels （P<0.01）. TJ structures were disrupted， and the expression of ZO-1， Occludin， and Claudin-1 was significantly reduced （P<0.05， P<0.01）. The protein expression levels of myosin light chain （MLC）， MLCK， phosphorylated （p）-MLC， and p-MLCK significantly increased （P<0.01）. Compared with the model group， all Qifu Lizhong decoction dose groups exhibited increased body weight， as well as significantly decreased DAI scores and histopathological scores （P<0.05， P<0.01）. The colonic levels of MPO， TNF-α， and IL-1β were significantly reduced （P<0.05， P<0.01）. In the Qifu Lizhong decoction + inhibitor group， the expression of TJ proteins ZO-1， Occludin， and Claudin-1 significantly increased （P<0.01）， while the protein expression levels of MLC， MLCK， p-MLC， and p-MLCK were significantly reduced （P<0.01）. In vitro experiment results showed that， compared with the normal group， the TNF-α group exhibited disordered cytoskeletal architecture， weakened fluorescence signals of ZO-1， Occludin， and Claudin-1， and significantly elevated protein expression levels of MLC， MLCK， p-MLC， and p-MLCK （P<0.01）. Compared with the TNF-α group， the Qifu Lizhong decoction + inhibitor group restored the ordered arrangement of the F-actin cytoskeleton， normalized the expression and localization of TJ proteins ZO-1， Occludin， and Claudin-1， and significantly decreased the protein expression levels of MLC， MLCK， p-MLC， and p-MLCK （P<0.01）.ConclusionQifu Lizhong decoction may exert its therapeutic effects on UC by inhibiting the MLCK/p-MLC signaling pathway， thereby stabilizing TJ structure and repairing intestinal barrier integrity.Keywords：ulcerative colitis;Qifu Lizhong decoction;intestinal barrier;tight junction;myosin light chain kinase （MLCK）/phosphorylated myosin light chain （p-MLC） signaling pathway84|19|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
- Abstract：ObjectiveTo investigate the mechanism by which Luoshi Neiyi prescription treats endometriosis （EMs） through the Toll-like receptor 4 （TLR4）/nuclear factor-κB （NF-κB） signaling pathway.MethodsAnimal experiments were conducted with 50 female SD rats， which were randomized into a sham operation group （10 rats） and a modeling group （40 rats）. An autologous endometrial transplantation method was used for the modeling of EMs. The 36 successfully modeled rats were randomly allocated into four groups （n=9 each）： The model group， the low-dose （7.87 g·kg-1） Luoshi Neiyi prescription group， the high-dose （15.74 g·kg-1） Luoshi Neiyi prescription group， and the dienogest （0.20 mg·kg-1） group. The physiological status and ectopic lesion volumes of rats in each group were observed. Hematoxylin-eosin （HE） staining was used to observe the morphology of the eutopic endometrial tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of inflammatory factors including interleukin-1β （IL-1β） and prostaglandin E2 （PGE2） in the serum of EMs rats. Immunohistochemistry was used to detect the expression of matrix metalloproteinase-9 （MMP-9） and vascular endothelial growth factor A （VEGFA） in the eutopic endometrial tissue. Western blot was adopted to determine the protein levels of TLR4， myeloid differentiation factor 88 （MyD88）， phosphorylated nuclear factor-κB （p-NF-κB）/NF-κB， MMP-9， and VEGFA in the eutopic endometrial tissue. In the cell experiments， the cell-counting kit-8 （CCK-8） assay was employed to screen the optimal concentration of Luoshi Neiyi prescription-containing serum， and a scratch assay was performed to assess the migration ability of iheESCs cells. Interventions with Luoshi Neiyi prescription-containing serum， resatorvid （TAK-242， a TLR4 inhibitor）， and lipopolysaccharides （LPS， a TLR4 agonist） were conducted， and Western blot was used to detect the expression of proteins related to the TLR4/NF-κB signaling pathway.ResultsThis experiment successfully replicated 36 EMs rat models. Compared with the sham operation group， the model group exhibited visible ectopic lesions on the abdominal wall and an increase in the writhing response score （P<0.01）. Furthermore， HE staining revealed the model group exhibited a thickened eutopic epithelium， stromal cell disarrangement， and evident infiltration of inflammatory cells. In addition， the model group showed elevated serum levels of IL-1β and PGE2 （P<0.05， P<0.01）， increased positive expression of MMP-9 and VEGFA in the ectopic endometrial tissue （P<0.01）， and up-regulated protein levels of TLR4， MyD88， p-NF-κB/NF-κB， MMP-9， and VEGFA in the ectopic endometrial tissue （P<0.05， P<0.01）. Compared with the model group， all treatment groups exhibited a reduction in the ectopic lesion volume （P<0.01）. Furthermore， the writhing response scores were decreased in the high-dose Luoshi Neiyi prescription group and the dienogest group （P<0.05， P<0.01）. The pathological state of the ectopic endometrial tissue was alleviated to varying degrees in the treatment groups. Low-dose Luoshi Neiyi prescription reduced serum PGE2 levels， and high-dose Luoshi Neiyi prescription and dienogest decreased serum IL-1β and PGE2 levels in EMs rats （P<0.05， P<0.01）. The treatment groups showed decreased positive expression of MMP-9 and VEGFA in the ectopic endometrial tissue （P<0.05， P<0.01） and down-regulated protein levels of TLR4， MyD88， p-NF-κB/NF-κB， MMP-9， and VEGFA in the ectopic endometrial tissue （P<0.05， P<0.01）. The cell experiments showed that 5%， 10%， and 20% Luoshi Neiyi prescription-containing sera significantly reduced the viability and inhibited the migration of iheESCs. Compared with the control group， 5%， 10%， and 20% Luoshi Neiyi prescription-containing serum groups and the TAK-242 group showed reduced protein levels of TLR4， MyD88， p-NF-κB/NF-κB， MMP-9， and VEGFA （P<0.01）. Compared with the control group， the LPS group showed increased expression of the above proteins （P<0.01）. Compared with the LPS group， the LPS+5%， 10%， and 20% Luoshi Neiyi prescription-containing serum groups showed reduced expression of the above proteins （P<0.05， P<0.01）.ConclusionLuoshi Neiyi prescription may modulate the TLR4/NF-κB signaling pathway to reduce the inflammatory response and histopathological damage in the eutopic endometrium and suppress the adhesive， invasive， and angiogenic biological processes in the ectopic endometrial tissue， thereby exerting its therapeutic effect on EMs.Keywords：endometriosis;Luoshi Neiyi prescription;Toll-like receptor 4 （TLR4）/nuclear factor-κB （NF-κB） signaling pathway;inflammatory response17|3|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
Efficacy and Mechanism of Shenling Qushi Prescription in Treatment of Hyperuricaemia Mice AI Introduction
Abstract：ObjectiveTo investigate the urate-lowering effect of Shenling Qushi prescription in the mouse model of hyperuricaemia.MethodsSixty-three C57BL/6N mice were randomly assigned to the following groups （n=9）： Control， model， low-dose （6 g·kg-1） Shenling Qushi prescription， medium-dose （12 g·kg-1） Shenling Qushi prescription， high-dose （24 g·kg-1） Shenling Qushi prescription， medium-dose Shenling Qushi prescription plus febuxostat （12+0.003 g·kg-1）， and febuxostat （3 mg·kg-1）. A mouse model of persistent hyperuricaemia was established via intraperitoneal injection of potassium oxazolamide （250 mg·kg-1） combined with oral administration of allopurinol （300 mg·kg-1） over a 28-day period. Concurrently， the prescription was administered orally at the specified doses once daily for 21 consecutive days. Throughout the experiment， mouse body weight， food intake， water consumption， and urine output were measured and recorded. Kidney and liver indices were calculated. Renal histopathological changes were observed by haematoxylin and eosin staining. Serum uric acid （SUA） and urinary uric acid （UUA） levels， along with xanthine oxidase （XOD） and adenosine deaminase （ADA）， alanine aminotransferase （ALT） and aspartate aminotransferase （AST） activities， were determined. Real-time PCR was employed to assess the mRNA levels of urate anion transporter 1 （URAT1） and glucose transporter 9 （GLUT9） in the renal tissue， alongside those of XOD and ADA in the liver tissue. The protein levels of URAT1 and GLUT9 in the renal tissue were determined by Western blot.ResultsCompared with the normal group， model mice exhibited reduced food intake and body weight （P<0.01）， decreased water consumption yet increased urine output， no significant change in the liver index but increased kidney index （P<0.01）. Pathological findings revealed renal tissue damage including glomerular atrophy， epithelial cell detachment， and inflammatory cell infiltration. Furthermore， the model group exhibited elevated UUA and SUA levels （P<0.01）， enhanced activities of ALT， AST， XOD， and ADA in the liver tissue （P<0.05， P<0.01）， upregulated mRNA and protein levels of URAT1 and GLUT9 in the renal tissue （P<0.05）， alongside markedly elevated mRNA levels of XOD and ADA in the liver （P<0.01）. Compared with the model group， the Shenling Qushi prescription groups showed no significant changes in body weight or food intake， with water consumption and urine output remaining within normal ranges， alleviated glomerular atrophy， with reduced pathological damage such as inflammatory infiltration， declined UUA and SUA levels （P<0.01）， and increased activities of ALT， AST， XOD， and ADA in the serum （P<0.01）. Real-time PCR results demonstrated that Shenling Qushi prescription downregulated the mRNA levels of URAT1 and GLUT9 in the renal tissue （P<0.05， P<0.01） and XOD and ADA in the hepatic tissue （P<0.05， P<0.01）. Western blot results demonstrated Shenling Qushi prescription reduced the protein levels of URAT1 and GLUT9 （P<0.05， P<0.01）.ConclusionShenling Qushi prescription modulates fluid balance and reduces uric acid levels， thereby alleviating renal injury in hyperuricaemic mice. This effect is highly likely mediated through inhibition of uric acid synthesis and reabsorption.Keywords：Shenling Qushi prescription;hyperuricemia;lowering of uric acid;pattern of spleen deficiency and dampness retention;drug efficacy12|2|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03- Abstract：ObjectiveTo investigate the intervention effect of Tengli Kangliu prescription （TKP） on the carcinogenesis of colorectal adenoma （CRA） induced by azoxymethane （AOM）/dextran sulphate sodium salt （DSS） in C57BL/6 mice and decipher the potential mechanism through regulating the signal transducer and activator of transcription 3 （STAT3） pathway to target M2-type macrophages.MethodsA total of 55 male C57BL/6 mice were randomized into a blank group （n=10）， a model group （n=15）， a celecoxib （0.02 g·kg-1·d-1） group （n=15）， a TKP （42.43 g·kg-1·d-1） group （n=15）. The mice in the model， TKP， and celecoxib groups were modeled for CRA lesions through the AOM/DSS three-cycle protocol. The intervention in each group began one week after free access to DSS and lasted for 12 weeks， and the blank group received 20 mL·kg-1·d-1 normal saline through gavage. Throughout the study period， changes in body mass and survival rate were recorded， alongside measurements of colorectal length and spleen mass. Histological changes of the colonic tissue were observed by HE staining. Immunohistochemical （IHC） staining was performed to detect the positive expression of CD68 and CD11c in the colorectal tissue. Western blot was employed to assess the protein levels of STAT3， phosphorylated （p）-STAT3， B-cell lymphoma 2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in the intestinal tissue. Real-time quantitative PCR was employed to analyze the mRNA levels of arginase 1 （Arg1）， CD206， and vascular endothelial growth factor （VEGF）. Enzyme-linked Immunosorbent assay（ELISA） was employed to measure the serum concentrations of Th2-type cytokines interleukin （IL）-4， IL-6， and IL-13 in mice.ResultsCompared with the blank group， the model group exhibited symptoms including diarrhea， hematochezia， and body mass loss， accompanied by shortened colon length， mucosal damage， and multiple tumors. In addition， the model group showcased up-regulated protein levels of STAT3， p-STAT3， and Bcl-2， down-regulated protein level of Bax， increased positive expression of CD68 and CD11c， and up-regulated mRNA levels of Arg1， CD206， and VEGF in the colon tissue， together with elevated serum levels of IL-4， IL-13， and IL-6 （P<0.05）. Compared with the model group， the above-mentioned indicators were partially reversed in both TKP group and celecoxib group， with superior effects observed in the TKP group （P<0.05）.ConclusionTKP significantly improves the survival quality of the mouse model of AOM/DSS-induced CRA by reducing intestinal inflammation and decreasing colorectal tumor number and size. It may delay the progression of AOM/DSS-induced colorectal tumor-like lesions by inhibiting activation of the STAT3/p-STAT3 signaling pathway in the intestinal tissue， targeting regulation of M2-type macrophages， and improving the tumor microenvironment， thereby suppressing CRA carcinogenesis.Keywords：colorectal adenoma （CRA）;precancerous lesion;colorectal cancer （CRC）;macrophages;Tengli Kangliu Prescription （TKP）108|24|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
Salviae Miltiorrhizae Radix et Rhizoma Extract Regulates Blood Pressure in Rat Model of Metabolic Hypertension Induced by High-sugan and High-fat Diet via TRPC3/6/NOX2/4 Sigraling Pathway Enhanced Publication AI Introduction
Abstract：ObjectiveTo explore the mechanisms of Salviae Miltiorrhizae Radix et Rhizoma in treating metabolic hypertension induced by a high-sugar and high-fat diet in rats based on network pharmacology， proteomics， and animal experiments.MethodsThirty male SD rats were randomized into the control， model， positive drug （tetrandrine， Tet， 50 mg·kg-1·d-1）， low-dose Salviae Miltiorrhizae Radix et Rhizoma （DS-L， 45×104 mg·kg-1·d-1）， and high-dose Salviae Miltiorrhizae Radix et Rhizoma （DS-H， 90×104 mg·kg-1·d-1） groups. Except for the control group， each group was fed a high-fat and high-sugar diet for 8 weeks for the modeling of metabolic hypertension. Following successful modeling， drug interventions were conducted through gavage for 4 weeks. Blood pressure and lipid indicators were monitored， and cardiac function was assessed via echocardiography. Samples from the thoracic aorta and cardiac tissue were collected for histopathological examination. Network pharmacology analysis identified key active components， potential targets， and mechanisms of Salviae Miltiorrhizae Radix et Rhizoma in treating hypertension. Proteomics technology was employed to analyze the differential proteins and major pathway targets to synergistically elucidate the antihypertensive mechanism of Salviae Miltiorrhizae Radix et Rhizoma. Ca2+ concentrations in the thoracic aorta and cardiac tissue were measured. The protein levels of transient receptor potential cation channel （TRPC）3， TRPC6， NADPH oxidase （NOX）2， and NOX4 were quantified via Western blotting. The levels of oxidative stress markers and inflammatory factors， including superoxide dismutase （SOD）， malondialdehyde （MDA）， tumor necrosis factor-α （TNF-α）， and interleukin-1β （IL-1β）， were determined by enzyme-linked immunosorbent assay （ELISA）. Molecular docking analysis was performed for the main components of Salviae Miltiorrhizae Radix et Rhizoma with TRPC3， TRPC6， NOX2， and NOX4.ResultsThe experimental results indicated that compared with the control group， the model group exhibited abnormally elevated blood pressure and increased lipid levels （P<0.01）. Compared with the model group， the DS-L group exhibited reduced systolic blood pressure （SBP）， diastolic blood pressure （DBP）， and mean arterial pressure （MAP） （P<0.05）， decreased serum levels of triglycerides （TG）， total cholesterol （TC）， and low-density lipoprotein cholesterol （LDL-C） （P<0.05）， and increased level of high-density lipoprotein cholesterol （HDL-C） （P<0.01）. The DS-H and Tet groups showed more significant effects （P<0.01）. Moreover， the interventions attenuated vascular wall thickening， myocardial cell injury， and collagen and lipid deposition. Network pharmacology and proteomics prediction results indicated that the core targets of Salviae Miltiorrhizae Radix et Rhizoma in treating hypertension were TRPC3， TRPC6， NOX2， and NOX4， and the core pathways included calcium signaling， cyclic guanosine monophosphate （cGMP）/cGMP-dependent protein kinase （PKG） signaling， and atherosclerosis-related pathways. The molecular mechanism experiment results indicated that compared with the control group， the model group exhibited significantly elevated tissue Ca2+ concentrations， exacerbated oxidative stress and inflammatory responses， and upregulated protein levels of TRPC3， TRPC6， NOX2， and NOX4 in the thoracic aorta and myocardial tissue （P<0.01）. Compared with the model group， DS-L reduced the free Ca2+ concentration， lowered the levels of IL-1β， TNF-α， SOD， and MDA （P<0.05）， and downregulated the protein levels of TRPC3， TRPC6， NOX2， and NOX4 in the thoracic aorta and myocardial tissue （P<0.05）. DS-H and Tet exhibited more significant effects （P<0.01）. Meanwhile， the main components of Salviae Miltiorrhizae Radix et Rhizoma had strong binding affinity with the core targets of hypertension.ConclusionSalviae Miltiorrhizae Radix et Rhizoma may ameliorate oxidative stress and mitigate inflammatory responses by regulating the TRPC3/6/NOX2/4 signaling pathway， thereby alleviating abnormal blood pressure abnormality and myocardial injury in hypertensive rats.Keywords：metabolic hypertension induced by a high-sugar and high-fat diet;Salviae Miltiorrhizae Radix et Rhizoma extract;transient receptor potential cation channel （TRPC）3/6/NADPH oxidase （NOX）2/4 signaling pathway;oxidative stress;inflammation17|5|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03A Multi-dimensional Indicator-based Approach for Quality Evaluation of Chinese Patent Medicines AI Introduction
Abstract：Chinese patent medicines are the core preparations for disease prevention and treatment in clinical traditional Chinese medicine （TCM）. Their quality is the key to ensuring safe and effective medication and promoting the high-quality development of the TCM industry. At present， the quality evaluation of Chinese patent medicines faces prominent problems， such as inadequate control of quality consistency， over-reliance on single indicators， one-sided evaluation dimensions， unstable statistical methods， and poor implementability of research findings. These defects lead to insufficient scientificity of evaluation results， making it difficult to support the implementation of policies including centralized procurement， high quality， and favorable prices for Chinese patent medicines. According to the core requirements of quality evaluation for Chinese patent medicines， this study established a four-dimensional comprehensive evaluation system encompassing consistency index（CI）， content index（MI）， effect index（EI）， and preparation index（PI）. All evaluation indicators were normalized to achieve horizontal comparability. Meanwhile， an improved radar chart was introduced to realize the visualization of evaluation results. This method can systematically integrate four types of core quality attributes： Quality consistency， component content， biological activity， and preparation characteristics. It can effectively distinguish quality differences among products of the same specification from different manufacturers. The evaluation results are unique， stable， and not affected by the addition or reduction of samples， which takes scientificity， objectivity， and operability into account. This method can provide scientific and technical support for screening high-quality Chinese patent medicines and implementing policies of centralized procurement， high quality， and favorable prices. Moreover， it has important practical significance for improving the quality evaluation system of Chinese patent medicines and advancing the standard and modern development of TCM.Keywords：Chinese patent medicine;quality consistency;quality evaluation;multi-dimensional comprehensive evaluation;improved radar chart67|11|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03- Abstract：ObjectiveTo establish a comprehensive evaluation framework combining multi-component quantification with daily intake in response to the challenges posed by multiple coexisting dosage forms， single-faceted quality evaluation， and ambiguous clinical equivalence of Huoxiang Zhengqi preparations， and to compare the quality differences and superiority among eight commercially available dosage forms.MethodsA total of 75 batches of Huoxiang Zhengqi preparations from 25 manufacturers were investigated. Ultra-performance liquid chromatography-triple quadrupole-tandem mass spectrometry （UPLC-QqQ-MS/MS） coupled with gas chromatography-triple quadrupole-tandem mass spectrometry （GC-QqQ-MS/MS） was adopted to simultaneously quantify 20 core marker components. Normalization was performed based on equivalent raw herb concentrations to eliminate interferences from dosage forms， excipients， and specifications. Considering the specified clinical dosage， the actual daily intake level was calculated to comprehensively evaluate component retention， content uniformity， and potential differences in in vivo exposure among different dosage forms.ResultsThe quality of Huoxiang Zhengqi preparations differed greatly among dosage forms and manufacturers. On the basis of the recommended daily doses in the package inserts， the total daily intake of the 20 tested components ranged from 3.14 to 614.30 mg·d-1， while that of hesperidin， a quality-control marker， ranged from 0.03 to 40.65 mg·d-1. Atractylodin was detected only in tinctures and soft capsules， with concentrations ranging from （2.68±0.01） to （5.73±0.37） mg·L-1. The soft capsules from manufacturer M22 had the highest atractylodin level， while atractylodin was not detected in the other dosage forms. Nucleosides were most abundant in the oral liquids and tinctures （M4 to M13）. The tincture from manufacturer M5 showed the highest nucleoside level of 29.12 mg·L-1， whereas the granules had the lowest nucleoside levels， with that of M23 being only 3.48 mg·L-1. Perillae Folium-related components varied greatly among batches， with an relative standard deviation （RSD） of 87.55%. The daily intake of hesperidin from all three granule products was below 3.6 mg·d-1， the reference value calculated for Huoxiang Zhengqi Shui according to the 2025 edition of the Chinese Pharmacopoeia.ConclusionThe levels of active components differed significantly among different dosage forms of Huoxiang Zhengqi preparations. Tinctures contained more types and higher overall levels of active components， while soft capsules were better at preserving volatile components. Granules and dripping pills had lower overall levels of active components. The comprehensive evaluation method established in this study can provide a basis for the quality control， process optimization， and the selection of high-quality products.Keywords：Huoxiang Zhengqi preparations;ultra-performance liquid chromatography-triple quadrupole-tandem mass spectrometry （UPLC-QqQ-MS/MS）;gas chromatography-triple quadrupole-tandem mass spectrometry （GC-QqQ-MS/MS）;multi-component quantification;quality evaluation71|17|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
Optimization of Characteristic Processing Technology for Polygalae Radix with Water Decoction of Coptidis Rhizoma from Jinling Medical School and Analysis of Its Chemical Constituent Variations Before and After Processing Enhanced Publication AI Introduction
Abstract：ObjectiveTo optimize the water extraction process of Coptidis Rhizoma （CR） and the processing of Polygalae Radix （PR） with the water decoction of CR， and to compare chemical constituents before and after processing.MethodsWith water volume， soaking time， decocting time， and decocting times as influencing factors， and the content of berberine， epiberberine， coptisine， jatrorrhizine， and palmatine and the yield of dry extract as evaluation indexes， the orthogonal test combined with multi-index comprehensive scoring method was employed to optimize the water extraction parameters of CR. With solid-liquid ratio， stir-frying temperature， and stir-frying time as influencing factors， and the content of tenuifolin， polygalaxanthone Ⅲ， and 3，6ʹ-disinapoyl sucrose and the yield of ethanol extract as evaluation indexes， the orthogonal test combined with multi-index comprehensive scoring method was applied to optimize the processing parameters of PR with the water decoction of CR. The differential chemical constituents of PR before and after processing were analyzed by ultra-performance liquid chromatography-quadrupole-Exactive Orbitrap-mass spectrometry （UPLC-Q Exactive Orbitrap MS）.ResultsThe optimal water extraction process of CR was as follows： Decocting for 3 times， 40 min each time， with 10 times the amount of water. The optimal processing technology of PR with the water decoction of CR was a solid-liquid ratio of 1∶1.5， a stir-frying temperature of 140 ℃， and stir-frying time of 20 min. A total of 31 differential components were identified before and after processing， including 17 components of PR and 15 components of CR. After processing， 14 new components such as coptisine， berberine， and palmatine emerged， and the content of arillanin A， glomeratose A， 3，6ʹ-disinapoyl sucrose， and ferulic acid was increased. The content of other intrinsic constituents of PR， such as onjisaponin D， polygalaxanthone Ⅺ， sibiricose A3， and tenuifoliside B， was generally decreased.ConclusionThe optimized characteristic processing technology of PR with the water decoction of CR is stable and feasible. Significant differences in chemical composition were observed between raw and processed PR. Processing with the water decoction of CR can effectively reduce the gastrointestinal irritant components originally present in PR while simultaneously introducing the bioactive constituents from CR. This study provides data support for the standardization research and mechanism elucidation of the ancient characteristic processing methods of the Jinling medical school.Keywords：Jinling medical school;characteristic processing;Polygalae Radix processed with the water decoction of Coptidis Rhizoma;process optimization;chemical constituents109|24|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Material Basis， Pharmacological Mechanisms， and Quality Control of Antitumor Effect of Cremastrae Pseudobulbus Pleiones Pseudobulbus： A Review Enhanced Publication AI Introduction
Abstract：Cremastrae Pseudobulbus Pleiones Pseudobulbus is a Chinese medicinal material used for clearing heat， detoxicifying， resolving phlegm， and dissipating nodules. It is derived from Cremastra appendiculata， Pleione bulbocodioides， or Pleione yunnanensis， as recorded in the 2025 edition of the Pharmacopoeia of the People′s Republic of China， with the former known as Maocigu and the latter two known as Bingqiuzi. Current antitumor studies mainly focus on polysaccharides， water-extracted alcohol-precipitated fractions， and purified extracts of C. appendiculata. Structurally characterized glucomannans suppress breast and liver tumor xenografts and exhibit immunomodulatory effects. The water-extracted alcohol-precipitated fractions inhibit tumor angiogenesis in hepatoma-bearing mice. A purified C. appendiculata extract standardized to five phenanthrene and bibenzyl constituents induces mitochondrial apoptosis in hepatocellular carcinoma cells. Reported pharmacological effects involve cell-cycle regulation， apoptosis， epithelial-mesenchymal transition， angiogenesis， autophagy， and the tumor immune microenvironment， with phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR）， Wnt/β-catenin， and Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathways being the major mechanism links. Quality evaluation of Cremastrae Pseudobulbus Pleiones Pseudobulbus has progressed from single-marker assays to an integrated approach involving botanical authentication， chromatographic fingerprinting， multicomponent analysis， and evaluation of associations between blood-absorbed constituents and antitumor effects. Militarine and dactylorhin A can be used for botanical identification and batch evaluation， and in vivo exposure data from related orchids are concentrated on militarine. Quantitative associations between these constituents and antitumor effects remain to be established. Clinical evidence mainly focuses on formula-based applications and expert experience. Comparative antitumor data in hepatoma models are available for the commercial specifications of Maocigu and Bingqiuzi， whereas parallel evaluations of pharmacological effects， safety windows， and drug interactions among the three official botanical origins remain insufficient. The major limitations are the incomplete standardization of botanical origins and preparations and the lack of quantitative links among quality markers， systemic exposure， antitumor effects， and toxicity endpoints， which constrain reproducible pharmacological evaluation and clinical translation of Cremastrae Pseudobulbus/Pleiones Pseudobulbus.Keywords：Cremastrae Pseudobulbus Pleiones Pseudobulbus;antitumor effect;material basis;pharmacological mechanism;quality control;quality marker92|14|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Discussion on Current Research Status and Developmental Paths of Animal Models Based on "Pattern Identification by Formula" Enhanced Publication AI Introduction
Abstract："Pattern identification by formula" originates from the formula-pattern correspondence theory in traditional Chinese medicine （TCM）， with its core being the reverse inference of the pattern attributes of models through pharmacodynamic responses after formula intervention. With the advancement of TCM modernization， stable and reliable pattern models have become an important bridge connecting basic research and clinical practice， and "pattern identification by formula" has provided a feasible approach to enhance the authenticity and clinical translational value of these models. In recent years， notable progress has been achieved in its application to single-pattern models （such as phlegm-stasis pattern， Yang deficiency pattern， and spleen-Qi deficiency pattern） as well as disease-pattern combination models involving the respiratory， digestive， circulatory， and nervous systems. It has not only verified the pattern attributes of the models but also revealed the pattern differentiation regularity of "different diseases with the same pattern" and "the same pattern treated with different formulas". On this basis， this study further conducts a commonality analysis of pattern models， summarizes them into two major categories （deficiency patterns and excess patterns）， and embodies the pathological connotation of "deficiency results from essence-Qi consumption， and excess arises from pathogen abundance". This not only reveals the internal connections between different models but also provides a basis for the summary of formula-pattern rules and research on pattern standardization. However， current studies still suffer multiple problems such as non-standardized naming of patterns， lack of rationality in modeling methods， simplified design of control experiments， and insufficient description of macroscopic patterns in evaluation indicators， which affect the scientific rigor and reproducibility of the research. Future research needs to promote the unification of nomenclature and evaluation criteria of patterns， optimize modeling methods， strengthen the design of control experiments， and establish a multi-dimensional model evaluation system integrating macro- and micro-level indicators. This aims to improve the rigor and strength of evidence for "pattern identification by formula" studies， strengthen interdisciplinary integration and clinical feedback， and promote the development of TCM pattern models towards standardization and scientification. This study not only provides theoretical reference and methodological support for improving the system of TCM pattern animal models but also offers an important pathway for the experimental interpretation and modernization of TCM theories.Keywords：pattern identification by formula;animal models;disease-pattern combination;research progress;formula-pattern correspondence109|16|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Iron Homeostasis Imbalance Promotes Atherosclerosis and Therapeutic Mechanisms of Traditional Chinese Medicine Enhanced Publication AI Introduction
Abstract：Iron is an indispensable trace element for the human body to maintain normal physiological functions， widely participating in key processes such as oxygen transport， energy metabolism， and cell signal transduction. The homeostasis of iron is crucial for maintaining the structural integrity and functional stability of the cardiovascular system. Recent studies have shown that iron homeostasis imbalance， especially iron overload， has become a major risk factor for the occurrence and development of atherosclerosis （AS）. The downstream-induced ferroptosis can form a "iron overload-lipid peroxidation-inflammation" vicious triangle through multiple pathways such as promoting oxidative stress， lipid peroxidation， and inflammatory response， and the three mutually reinforce each other to accelerate plaque formation and progression. Traditional Chinese medicine （TCM） has demonstrated unique advantages in the prevention and treatment of AS， with definite clinical efficacy. Its mechanism of action， in addition to improving lipid metabolism and protecting vascular endothelium， is closely related to the regulation of iron homeostasis in the body. From the new perspectives of systemic iron homeostasis imbalance and the "iron overload-lipid peroxidation-inflammation" vicious triangle， this article reviews the research progress in the association between iron homeostasis imbalance and AS in recent years， and integrate the mechanism of iron homeostasis imbalance in modern medicine with the TCM theory of stasis and toxin interconnection. It focuses on exploring the potential molecular mechanisms of TCM in regulating iron homeostasis through intervention in key pathways of iron overload and inhibition of ferroptosis， summarizes the "iron reduction-antioxidation-anti-inflammation" network constructed by TCM compound prescriptions， and the characteristics of TCM active components in synergistically resisting systemic iron homeostasis imbalance through sharing key targets such as nuclear factor erythroid 2-related factor 2 （Nrf2） and nuclear factor （NF）-κB. This article provides ideas and a theoretical basis that combine the characteristics of TCM theory with modern scientific evidence for the prevention and treatment of AS.Keywords：iron homeostasis;atherosclerosis;traditional Chinese medicine;oxidative stress;inflammation14|2|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03- Abstract：Chronic atrophic gastritis （CAG）， a premalignant gastric condition， represents a critical stage in inflammation-cancer transformation. In this pathological process， mitochondrial damage serves as a key mediator in the inflammation-driven transformation of normal gastric mucosal epithelial cells into gastric cancer cells， while the dysregulation of the reactive oxygen species （ROS）/NOD-like receptor protein 3 （NLRP3） axis plays a key role in perpetuating the vicious cycle of inflammation-mitochondrial damage. The classical theory of traditional Chinese medicine （TCM）， vigorous fire consuming Qi， aptly encapsulates this pathological feature. The essence of this theory lies in the struggle between pathogenic and vital factors， wherein vigorous fire shares similarities with chronic inflammation and may be regarded as a driving force behind inflammation-cancer transformation. Qi reflects the mitochondrial function， and consuming Qi signifies structural and functional impairment of mitochondria. Thus， this theory accurately summarizes the pathological characteristics of inflammation-mitochondrial damage during CAG progression. Building upon this theoretical framework， the theory of vigorous fire consuming Qi provides a holistic understanding of CAG pathogenesis. Reviewing the clinical expertise of TCM master YANG Chunbo in treating spleen-stomach disorders， this paper further elucidates its therapeutic implications： modulating systemic inflammatory responses to restore gastric mucosal homeostasis and targeting mitochondrial damage as a pivotal intervention to delay CAG progression. Clinically， achieving dynamic equilibrium between fire and Qi is essential， mitigating excessive inflammation without compromising vital Qi， while reinforcing Qi without exacerbating pathological fire. This approach offers novel insights for developing preventive and therapeutic strategies against CAG.Keywords：chronic atrophic gastritis;vigorous fire consuming Qi;inflammation;mitochondria damage;reactive oxygen species （ROS）/NOD-like receptor protein 3 （NLRP3）64|15|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
Application of Mass Spectrometry Imaging in Research on Material Basis of Traditional Chinese Medicine： A Review AI Introduction
Abstract：The scientific connotation of the material basis of traditional Chinese medicine （TCM） depends not only on the composition and abundance of its constituents， but more critically on their spatial distribution within medicinal materials and in vivo. However， conventional analytical approaches have limited capacity to resolve in situ spatial information， failing to delve into therapeutic mechanisms of complex TCM systems. Mass spectrometry imaging （MSI） enables label-free in situ analysis with spatial visualization of multiple constituents， providing essential technical support for investigations into the material basis of TCM. In recent years， the application of MSI has continuously expanded across studies of single medicinal materials， processing， compound preparations， and in vivo distribution， systematically elucidating microscale spatial distribution patterns of TCM constituents. Accumulating evidence indicates that MSI facilitates clarification of the relationships among endogenous constituents， biosynthetic pathways， medicinal parts， and geo-authenticity （Daodi）. Moreover， MSI can dynamically depict spatiotemporal transformation of constituents during processing， offering intuitive evidence for the mechanisms underlying toxicity reduction and efficacy enhancement. In the studies of compound preparations， MSI can resolve microregional distribution characteristics of diverse constituents and their potential interactions， thereby deepening the understanding of compatibility principles. In addition， MSI demonstrates unique advantages in in situ tracing of constituents in vivo， as well as in spatially informed quality evaluation and authentication/adulteration identification. Overall， MSI is driving a shift in the research on the material basis of TCM from conventional compositional profiling toward spatial-functional elucidation， providing important technical support for establishing "material-space-efficacy" relationships. Despite remaining challenges in quantification， spatial resolution， and data processing， MSI shows broad promise for application in modern TCM research.Keywords：traditional Chinese medicine （TCM）;mass spectrometry imaging （MSI）;material basis;spatial distribution;application prospect12|2|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Research Progress on Pathogenesis and Targeted Intervention Strategies of Chinese Herbal Active Components in Autism Spectrum Disorder： A Review Enhanced Publication AI Introduction
Abstract：Autism Spectrum Disorder （ASD） is a neurodevelopmental disorder with rapidly increasing global prevalence， characterized by core symptoms of social communication deficits and stereotyped repetitive behaviors. Although genetic predisposition， abnormal epigenetic regulation， perinatal environmental exposure， and nutritional-metabolic imbalances are recognized as major risk factors， the precise etiological mechanisms remain incompletely understood. Current clinical management primarily relies on behavioral interventions， with limited pharmacological options accompanied by adverse effects. Recent studies have demonstrated the unique therapeutic value of active components from Chinese herbal medicine in ASD intervention. This article reviews the mechanisms underlying various Chinese herbal active components in ASD treatment， including improvements in synaptic dysfunction， blood-brain barrier impairment， neurotransmitter regulation， cerebellar dysfunction， immune dysregulation and neuroinflammation， oxidative stress， programmed neuronal cell death， and lipid metabolism. These bioactive components exhibit multi-target and multi-pathway regulatory effects， providing novel therapeutic strategies and directions for ASD.Keywords：autism;active components of Chinese herbal medicine;oxidative stress;ferroptosis;synapse;baicalin84|15|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Traditional Chinese Medicine Treatment of Liver Cancer Based on Hippo Signaling Pathway： A Review Enhanced Publication AI Introduction
Abstract：Liver cancer， as a malignant digestive tract tumor with high incidence and mortality rates globally， has witnessed continuous increases in both incidence and mortality in recent years. Although modern medical treatment methods have achieved certain results in disease control， the treatment of liver cancer remains challenging due to the low early diagnosis rate， obvious toxic and side effects， and widespread drug resistance. Against this backdrop， exploring more efficient and safer treatment strategies is of utmost urgency. The Hippo cascade signaling pathway plays a crucial regulatory role in processes such as the proliferation， differentiation， apoptosis， and invasion of liver cancer cells. It is extensively involved in the occurrence and development of liver cancer， serving as an important target for anti-liver cancer treatment research. Traditional Chinese medicine （TCM） can exert anti-liver cancer effects through multiple approaches， mechanisms， and pathways. It has shown remarkable efficacy in preventing postoperative recurrence and metastasis of liver cancer， reducing adverse reactions of radiotherapy and chemotherapy， and improving the quality of life， thus becoming a key component of comprehensive liver cancer treatment. Studies have confirmed that the TCM active components including flavonoids， alkaloids， terpenoids， polyphenols， saponins， and quinones， as well as the TCM compound prescriptions such as compound Banmao capsules， Erzhu Jiedu decoction， Pianzaihuang， and Zhenggan prescription， can effectively regulate the Hippo signaling pathway. They exert significant anti-liver cancer effects through multiple mechanisms， such as inducing autophagy and apoptosis of liver cancer cells， improving macrophage polarization， blocking epithelial-mesenchymal transition， inhibiting glycolytic metabolism， promoting immune cell activation， reversing tumor drug resistance， and arresting the cell cycle. This study used "liver cancer" "Hippo" "signaling pathway" and "traditional Chinese medicine" as the main keywords to search multiple literature databases， including PubMed， CNKI， and VIP. By discussing and analyzing the mechanisms of TCM in regulating the Hippo signaling pathway for the treatment of liver cancer in the past five years， this paper aims to provide ideas and references for the research and development of new anti-liver cancer drugs in clinical practice.Keywords：Hippo;signal pathway;traditional Chinese medicine;liver cancer;research progress101|17|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Active Compounds and Modern Pharmacological Effect of Armeniacae Semen Amarum： A Review Enhanced Publication AI Introduction
Abstract：Armeniacae Semen Amarum， the dried mature seeds of plants such as Prunus armeniaca var. ansu （Rosaceae）， have a long history for medicinal use. Modern research indicates that the core active compounds of Armeniacae Semen Amarum， such as amygdalin， fatty acids， and volatile oils， exhibit multiple pharmacological effects including antitussive， bronchodilatory， anti-inflammatory， antioxidant， antitumor， antifibrotic， and immunomodulatory effects. Consequently， their potential applications in treating respiratory diseases， tumors， tissue injury， and metabolic disorders have garnered significant attention. However， a systematic integrated analysis of the relationship between the traditional efficacy， modern pharmacology， key material basis， and multi-pathway mechanisms of Armeniacae Semen Amarum remains lacking. Using bibliometric methods combined with CiteSpace visualization technology， this study systematically summarizes the research hotspots on Armeniacae Semen Amarum and its representative component amygdalin， including the key roles in inflammation regulation， apoptosis induction， cell cycle arrest， oxidative stress balance， and fibrosis modulation. This article reviews the research progress in Armeniacae Semen Amarum across from four major dimensions—traditional applications， visualization analysis， material basis， and modern pharmacological studies， providing a reference for the further basic and clinical studies of Armeniacae Semen Amarum in respiratory diseases， oncology， and immune-related disorders.Keywords：Armeniacae Semen Amarum;amygdalin;antitussive and bronchodilatory effects;anti-inflammatory effects;oxidative stress;antitumor effect20|2|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03Chemical Components and Pharmacological Effects of Lianpo Yin： A Review of Ancient and Modern Literature AI Introduction
Abstract：Lianpo Yin was first recorded in the Revised Treatise on Cholera from Suixi Residence by WANG Mengying. It is composed of seven medicinal herbs： Coptidis Rhizoma， Magnoliae Officinalis Cortex， Sojae Semen Praeparatum， Acori Tatarinowii Rhizoma， Pinelliae Rhizoma， Gardeniae Fructus， and Phragmitis Rhizoma. As one of the classic prescriptions for clearing heat， resolving dampness， regulating Qi， and harmonizing the middle energizer， it has been included in the Catalogue of Ancient Classic Prescriptions （Second Batch： Han Chinese Medicine） published by the National Administration of Traditional Chinese Medicine in 2023. Lianpo Yin is primarily indicated for cholera caused by the accumulation of dampness-heat， and it can promote digestion and eliminate phlegm. By summarizing the ancient literature records， chemical constituents of individual herbs and the compound formula， pharmacological effects， and modern clinical applications of Lianpo Yin， this paper discovers that the understandings of most ancient physicians are consistent with the original text. The pathogenesis treated by this prescription is generally attributed to the accumulation of dampness-heat in the middle energizer and disrupted ascending and descending of Qi. The main chemical components of this prescription include coptisine， trigonelline， genistein， palmatine， berberine， honokiol， and magnolol. Lianpo Yin exhibits pharmacological effects such as anti-inflammatory activity， regulation of apoptosis， modulation of mitochondrial autophagy， regulation of the hypothalamic-pituitary-adrenal （HPA） axis， promotion of gastrointestinal motility， improvement of the gastric mucosal barrier， regulation of intestinal flora and their metabolites， and antimicrobial activity. In modern clinical practice， this prescription is mainly used to treat digestive system diseases such as chronic superficial gastritis and Helicobacter pylori （Hp）-associated gastritis. Additionally， it demonstrates significant therapeutic effects on various diseases affecting the nervous， respiratory， dermatological， and cardiovascular systems. This study provides a detailed review of the ancient literature records， chemical components， pharmacological effects， and clinical applications of Lianpo Yin and its modified formulas， aiming to offer references for the dosage form development and broader clinical application of this classic prescription.Keywords：Lianpo Yin;chemical components;pharmacological effects;ancient and modern literature;research progress8|2|0<HTML><H-PDF> <L-PDF>Updated：2026-09-03
