Hyperoside Alleviates -Induced Gastric Epithelial Cell Injury by Regulating Nrf2/HO-1 Signaling.

Infection with is the major causative factor of chronic gastritis, peptic ulcer, gastric cancer, and other diseases. Gastric mucosal epithelial injury characterized by abnormal apoptosis, oxidative stress, and inflammation is a crucial mechanism of infection. Hyperoside (HYP) is a flavonol glycoside derived from many herbal plants, which exhibits potent anti-apoptotic, antioxidant, and anti-inflammatory properties. Our research explored whether it exerts protective effects on -infected human gastric epithelial cells. GES-1 cells were first treated for 24 h with HYP (0, 10, 20, 40, 80, 100, or 120 μM) to determine the cytotoxicity of HYP. Subsequently, GES-1 cells were pre-treated for 4 h with HYP (80 μM), followed by exposure to for 24 h. CCK-8 assay, flow cytometry assay, ELISA, RT-qPCR, DCFH-DA staining, the commercial assay kits, immunofluorescence staining, and western blotting were used to assess cell viability, cell apoptosis, pro-inflammatory cytokine levels, oxidative stress marker levels, and Nrf2/HO-1 signaling-related molecule levels. The Nrf2 inhibitor ML385 was employed to verify the beneficial role of Nrf2 activation in HYP-mediated GES-1 cell injury induced by . The results showed that HYP pre-treatment reversed -induced cell apoptosis, inflammation, and oxidative stress in GES-1 cells. Furthermore, HYP downregulated Nrf2, HO-1, and NQO1 protein levels in -infected GES-1 cells. ML385 overturned the protective effects of HYP against -induced GES-1 cell apoptosis, inflammation, and oxidative stress. In conclusion, HYP protects gastric epithelial cells against -induced cell injury by activating the Nrf2/HO-1 pathway.