幽门螺杆菌（H. pylori）感染可引起胃上皮细胞广泛凋亡，是慢性胃炎、胃肠道化生、不典型胃增生向胃癌进展的关键催化剂。及时根除幽门螺杆菌对于改善与胃粘膜慢性炎症相关的病理生理状况和胃癌的一级预防至关重要。金合欢素具有多方面的药理活性，如抗癌、抗炎和抗氧化特性，已在各个领域进行了广泛的研究。然而，金合欢素对H. pylori感染的胃粘膜上皮细胞的影响及作用机制尚不清楚。 探讨金合欢素对H. pylori感染的GES-1细胞凋亡的防御作用并探讨其作用机制。在体外用幽门螺杆菌和金合欢素处理 GES-1 细胞。使用 CCK-8 测定评估细胞活力，通过乳酸脱氢酶测定评估细胞死亡率，通过伤口愈合测定评估细胞迁移和愈合能力的变化，通过流式细胞术和 TUNEL 染色评估细胞凋亡率，以及细胞凋亡相关蛋白的表达水平通过蛋白质印迹分析。H. pylori感染导致GES-1细胞活力下降、细胞死亡率增加、细胞迁移受到抑制、细胞凋亡率增加、Bax和cle-caspase3表达增加、Bcl-2表达减少。相反，金合欢素处理可增强细胞活力，减轻幽门螺杆菌感染诱导的细胞凋亡，并通过上调 Bcl-2 和下调 Bax 和 cleaved caspase-3 来调节凋亡调节蛋白的表达。金合欢素显着提高 GES-1 细胞活力并抑制细胞凋亡抑制H. pylori感染的GES-1细胞凋亡，从而对胃粘膜上皮细胞发挥保护作用。©作者2024。百事登出版集团出版。保留所有权利。

Helicobacter pylori (H. pylori) infection can cause extensive apoptosis of gastric epithelial cells, serving as a critical catalyst in the progression from chronic gastritis, gastrointestinal metaplasia, and atypical gastric hyperplasia to gastric carcinoma. Prompt eradication of H. pylori is paramount for ameliorating the pathophysiological conditions associated with chronic inflammation of the gastric mucosa and the primary prevention of gastric cancer. Acacetin, which has multifaceted pharmacological activities such as anti-cancer, anti-inflammatory, and antioxidative properties, has been extensively investigated across various domains. Nevertheless, the impact and underlying mechanisms of action of acacetin on H. pylori-infected gastric mucosal epithelial cells remain unclear.To explore the defensive effects of acacetin on apoptosis in H. pylori-infected GES-1 cells and to investigate the underlying mechanisms.GES-1 cells were treated with H. pylori and acacetin in vitro. Cell viability was assessed using the CCK-8 assay, cell mortality rate via lactate dehydrogenase assay, alterations in cell migration and healing capacities through the wound healing assay, rates of apoptosis via flow cytometry and TUNEL staining, and expression levels of apoptosis-associated proteins through western blot analysis.H. pylori infection led to decreased GES-1 cell viability, increased cell mortality, suppressed cell migration, increased rate of apoptosis, increased expressions of Bax and cle-caspase3, and decreased Bcl-2 expression. Conversely, acacetin treatment enhanced cell viability, mitigated apoptosis induced by H. pylori infection, and modulated the expression of apoptosis-regulatory proteins by upregulating Bcl-2 and downregulating Bax and cleaved caspase-3.Acacetin significantly improved GES-1 cell viability and inhibited apoptosis in H. pylori-infected GES-1 cells, thereby exerting a protective effect on gastric mucosal epithelial cells.©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.