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.