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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

Yangweishu Ameliorates Chronic Atrophic Gastritis with Stomach Yin Deficiency Syndrome Through IL-6/STAT3 Signaling Pathway.

作者信息

Jiao Zhiyong, Zheng Jia, Yang Xinyu, Ruan Qin, Ma Yuhan, Huang Yuzhe, Jin Cheng, Gui Shuangying, Xuan Zihua, Liang Juan, Jia Xiaoyi

机构信息

School of Pharmacy, Anhui University of Chinese Medicine, Hefei, 230012, People's Republic of China.

Anhui Province Key Laboratory of Bioactive Natural Products, Hefei, 230012, People's Republic of China.

出版信息

Drug Des Devel Ther. 2025 Sep 8;19:7865-7885. doi: 10.2147/DDDT.S529330. eCollection 2025.

DOI:10.2147/DDDT.S529330
PMID:40969849
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12441957/
Abstract

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.

摘要

背景

胃阴虚证慢性萎缩性胃炎（YDCAG）是一种以胃黏膜炎症和胃腺细胞萎缩为特征的癌前病变。养胃舒（YWS）被广泛用于治疗胃肠道疾病。

目的

本研究旨在探讨YWS治疗YDCAG的作用机制。

方法

采用综合造模方法建立YDCAG大鼠模型，并用MNNG刺激诱导人胃上皮细胞（GES-1）损伤模型。进行苏木精-伊红染色（HE）、酶联免疫吸附测定（ELISA）、实时聚合酶链反应（RT-PCR）、免疫组织化学和蛋白质印迹法，以观察YWS对YDCAG大鼠和GES-1细胞的影响。运用网络药理学确定参与YWS抗YDCAG作用的潜在核心靶点和信号通路。采用RT-PCR和蛋白质印迹法检测体内外IL-6/STAT3信号通路中的基因和蛋白表达。通过流式细胞术、免疫荧光、RT-PCR和蛋白质印迹法评估GES-1细胞中的凋亡情况。

结果

YWS显著改善了YDCAG大鼠的胃形态，并减轻了MNNG诱导的GES-1细胞损伤。YWS治疗还降低了炎症细胞因子的血清、组织和细胞水平，同时增强了抗氧化能力。网络药理学分析表明，YWS调节细胞凋亡并抑制IL-6/STAT3信号通路。此外，YWS对细胞凋亡具有改善作用，并在体内外抑制IL-6/STAT3信号通路基因和蛋白的表达。

结论

YWS对YDCAG具有良好的治疗效果，这可能与抑制IL-6/STAT3信号通路密切相关。

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