Weifuchun alleviates MNNG-induced gastric epithelial cell injury via TGF-β1/PI3K/Akt pathway

Chronic atrophic gastritis (CAG), a chronic form of gastritis, is critical in the early stages of stomach precancerous lesions. Delving into the origins of chronic atrophic gastritis and conducting drug screenings is crucial. However, the precise mechanisms by which Weifuchun protects gastric mucosal epithelial cells remain incompletely understood. This project's objective is to investigate the potential mechanisms by which Weifuchun safeguards gastric mucosal epithelial cells from harm. We mimicked the CAG process by MNNG-induced injury of gastric mucosal epithelial cells (GES-1) and detected changes in cell activity, apoptosis, cell cycle and migration and invasion. Changes in cellular epithelial-mesenchymal transition (EMT), PI3K/AKT pathway proteins and inflammatory factors were detected. Exploring how Weifuchun influences the biological actions of GES-1 induced by MNNG. Then, pharmacological rescue experiments were performed by treatment with TGF-β1/PI3K/AKT inhibitors. MNNG induced GES-1 to undergo cellular aggressive transformation, including proliferation, invasion, and EMT. Weifuchun significantly ameliorated MNNG-induced damage to GES-1, with the effects of this treatment being regulated by the TGF-β1 and PI3K/Akt pathways. The results demonstrated that Weifuchun has the potential to mitigate MNNG-induced inflammatory injury and aggressive transformation of gastric epithelial cells by modulating the TGF-β1/PI3K/AKT pathway. This suggests potential new perspectives and approaches for future research into the prevention and management of gastric cancer.