Wang Yanfen, Liu Yuxue, Zheng Xiuhua
Department of Basic Medicine, Henan Vocational College of Nursing, Anyang, China.
College of Life Science, Henan Normal University, Xinxiang, China.
Pol J Microbiol. 2025 Mar 26;74(1):60-70. doi: 10.33073/pjm-2025-005. eCollection 2025 Mar 1.
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.
感染是慢性胃炎、消化性溃疡、胃癌及其他疾病的主要致病因素。以异常凋亡、氧化应激和炎症为特征的胃黏膜上皮损伤是感染的关键机制。金丝桃苷（HYP）是一种从多种草药植物中提取的黄酮醇苷，具有强大的抗凋亡、抗氧化和抗炎特性。我们的研究探讨了它是否对感染的人胃上皮细胞具有保护作用。首先用HYP（0、10、20、40、80、100或120μM）处理GES-1细胞24小时，以确定HYP的细胞毒性。随后，用HYP（80μM）预处理GES-1细胞4小时，然后暴露于 24小时。采用CCK-8检测、流式细胞术检测、ELISA、RT-qPCR、DCFH-DA染色、商业检测试剂盒、免疫荧光染色和蛋白质印迹法来评估细胞活力、细胞凋亡、促炎细胞因子水平、氧化应激标志物水平以及Nrf2/HO-1信号相关分子水平。使用Nrf2抑制剂ML385来验证Nrf2激活在介导的HYP诱导的GES-1细胞损伤中的有益作用。结果表明，HYP预处理可逆转诱导的GES-1细胞凋亡、炎症和氧化应激。此外，HYP下调了感染的GES-1细胞中Nrf2、HO-1和NQO1蛋白水平。ML385推翻了HYP对诱导的GES-1细胞凋亡、炎症和氧化应激的保护作用。总之，HYP通过激活Nrf2/HO-1途径保护胃上皮细胞免受诱导的细胞损伤。
