{"title":"养胃舒通过IL-6/STAT3信号通路改善胃阴虚证慢性萎缩性胃炎","authors":"Zhiyong Jiao, Jia Zheng, Xinyu Yang, Qin Ruan, Yuhan Ma, Yuzhe Huang, Cheng Jin, Shuangying Gui, Zihua Xuan, Juan Liang, Xiaoyi Jia","doi":"10.2147/DDDT.S529330","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Chronic atrophic gastritis of stomach yin deficiency syndrome (YDCAG) is a precancerous lesion characterized by inflammation of gastric mucosa and atrophy of gastric adenocytes. Yangweishu (YWS) is widely used to treat gastrointestinal diseases.</p><p><strong>Objective: </strong>This study was to investigate the mechanism of YWS in YDCAG.</p><p><strong>Methods: </strong>The YDCAG rat model was established using a comprehensive modeling approach, and a human gastric epithelial cell (GES-1) injury model was induced by MNNG stimulation. Hematoxylin-eosin staining (HE), enzyme-linked immunosorbent assay (ELISA), real-time polymerase chain reaction (RT-PCR), immunohistochemistry and Western blotting were performed to observe the effects of YWS on YDCAG rats and GES-1 cells. Network pharmacology was conducted to identify potential core targets and signaling pathways involved in the anti-YDCAG effects of YWS. RT-PCR and Western blotting were employed to measure the gene and protein expression in the IL-6/STAT3 signaling pathway in vivo and in vitro. Apoptosis in GES-1 cells was evaluated through flow cytometry, immunofluorescence, RT-PCR, and Western blotting.</p><p><strong>Results: </strong>YWS significantly improved gastric morphology in YDCAG rats and alleviated GES-1 cell injury induced by MNNG. YWS treatment also reduced serum, tissue, and cellular levels of inflammatory cytokines, while enhancing antioxidant capacity. Network pharmacology analysis suggested that YWS modulates apoptosis and inhibits the IL-6/STAT3 signaling pathway. Furthermore, YWS has an ameliorative effect on apoptosis and inhibits the expression of IL-6/STAT3 signaling pathway genes and proteins in vitro and in vivo.</p><p><strong>Conclusion: </strong>YWS has a good therapeutic effect on YDCAG, which may be closely related to the inhibition of IL-6/STAT3 signaling pathway.</p>","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"7865-7885"},"PeriodicalIF":5.1000,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12441957/pdf/","citationCount":"0","resultStr":"{\"title\":\"Yangweishu Ameliorates Chronic Atrophic Gastritis with Stomach Yin Deficiency Syndrome Through IL-6/STAT3 Signaling Pathway.\",\"authors\":\"Zhiyong Jiao, Jia Zheng, Xinyu Yang, Qin Ruan, Yuhan Ma, Yuzhe Huang, Cheng Jin, Shuangying Gui, Zihua Xuan, Juan Liang, Xiaoyi Jia\",\"doi\":\"10.2147/DDDT.S529330\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Chronic atrophic gastritis of stomach yin deficiency syndrome (YDCAG) is a precancerous lesion characterized by inflammation of gastric mucosa and atrophy of gastric adenocytes. Yangweishu (YWS) is widely used to treat gastrointestinal diseases.</p><p><strong>Objective: </strong>This study was to investigate the mechanism of YWS in YDCAG.</p><p><strong>Methods: </strong>The YDCAG rat model was established using a comprehensive modeling approach, and a human gastric epithelial cell (GES-1) injury model was induced by MNNG stimulation. Hematoxylin-eosin staining (HE), enzyme-linked immunosorbent assay (ELISA), real-time polymerase chain reaction (RT-PCR), immunohistochemistry and Western blotting were performed to observe the effects of YWS on YDCAG rats and GES-1 cells. Network pharmacology was conducted to identify potential core targets and signaling pathways involved in the anti-YDCAG effects of YWS. RT-PCR and Western blotting were employed to measure the gene and protein expression in the IL-6/STAT3 signaling pathway in vivo and in vitro. Apoptosis in GES-1 cells was evaluated through flow cytometry, immunofluorescence, RT-PCR, and Western blotting.</p><p><strong>Results: </strong>YWS significantly improved gastric morphology in YDCAG rats and alleviated GES-1 cell injury induced by MNNG. YWS treatment also reduced serum, tissue, and cellular levels of inflammatory cytokines, while enhancing antioxidant capacity. Network pharmacology analysis suggested that YWS modulates apoptosis and inhibits the IL-6/STAT3 signaling pathway. Furthermore, YWS has an ameliorative effect on apoptosis and inhibits the expression of IL-6/STAT3 signaling pathway genes and proteins in vitro and in vivo.</p><p><strong>Conclusion: </strong>YWS has a good therapeutic effect on YDCAG, which may be closely related to the inhibition of IL-6/STAT3 signaling pathway.</p>\",\"PeriodicalId\":11290,\"journal\":{\"name\":\"Drug Design, Development and Therapy\",\"volume\":\"19 \",\"pages\":\"7865-7885\"},\"PeriodicalIF\":5.1000,\"publicationDate\":\"2025-09-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12441957/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Drug Design, Development and Therapy\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.2147/DDDT.S529330\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q1\",\"JCRName\":\"CHEMISTRY, MEDICINAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Drug Design, Development and Therapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2147/DDDT.S529330","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"CHEMISTRY, MEDICINAL","Score":null,"Total":0}
Yangweishu Ameliorates Chronic Atrophic Gastritis with Stomach Yin Deficiency Syndrome Through IL-6/STAT3 Signaling Pathway.
Background: Chronic atrophic gastritis of stomach yin deficiency syndrome (YDCAG) is a precancerous lesion characterized by inflammation of gastric mucosa and atrophy of gastric adenocytes. Yangweishu (YWS) is widely used to treat gastrointestinal diseases.
Objective: This study was to investigate the mechanism of YWS in YDCAG.
Methods: The YDCAG rat model was established using a comprehensive modeling approach, and a human gastric epithelial cell (GES-1) injury model was induced by MNNG stimulation. Hematoxylin-eosin staining (HE), enzyme-linked immunosorbent assay (ELISA), real-time polymerase chain reaction (RT-PCR), immunohistochemistry and Western blotting were performed to observe the effects of YWS on YDCAG rats and GES-1 cells. Network pharmacology was conducted to identify potential core targets and signaling pathways involved in the anti-YDCAG effects of YWS. RT-PCR and Western blotting were employed to measure the gene and protein expression in the IL-6/STAT3 signaling pathway in vivo and in vitro. Apoptosis in GES-1 cells was evaluated through flow cytometry, immunofluorescence, RT-PCR, and Western blotting.
Results: YWS significantly improved gastric morphology in YDCAG rats and alleviated GES-1 cell injury induced by MNNG. YWS treatment also reduced serum, tissue, and cellular levels of inflammatory cytokines, while enhancing antioxidant capacity. Network pharmacology analysis suggested that YWS modulates apoptosis and inhibits the IL-6/STAT3 signaling pathway. Furthermore, YWS has an ameliorative effect on apoptosis and inhibits the expression of IL-6/STAT3 signaling pathway genes and proteins in vitro and in vivo.
Conclusion: YWS has a good therapeutic effect on YDCAG, which may be closely related to the inhibition of IL-6/STAT3 signaling pathway.
期刊介绍：
Drug Design, Development and Therapy is an international, peer-reviewed, open access journal that spans the spectrum of drug design, discovery and development through to clinical applications.
The journal is characterized by the rapid reporting of high-quality original research, reviews, expert opinions, commentary and clinical studies in all therapeutic areas.
Specific topics covered by the journal include:
Drug target identification and validation
Phenotypic screening and target deconvolution
Biochemical analyses of drug targets and their pathways
New methods or relevant applications in molecular/drug design and computer-aided drug discovery*
Design, synthesis, and biological evaluation of novel biologically active compounds (including diagnostics or chemical probes)
Structural or molecular biological studies elucidating molecular recognition processes
Fragment-based drug discovery
Pharmaceutical/red biotechnology
Isolation, structural characterization, (bio)synthesis, bioengineering and pharmacological evaluation of natural products**
Distribution, pharmacokinetics and metabolic transformations of drugs or biologically active compounds in drug development
Drug delivery and formulation (design and characterization of dosage forms, release mechanisms and in vivo testing)
Preclinical development studies
Translational animal models
Mechanisms of action and signalling pathways
Toxicology
Gene therapy, cell therapy and immunotherapy
Personalized medicine and pharmacogenomics
Clinical drug evaluation
Patient safety and sustained use of medicines.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
