Effect of acacetin on inhibition of apoptosis in Helicobacter pyloriinfected gastric epithelial cell line  

作　　者：Qi-Xi Yao Zi-Yu Li Hou-Le Kang Xin He Min Kang 

机构地区：[1]Department of Gastroenterology,The Affiliated Hospital of Southwest Medical University,Luzhou 646000,Sichuan Province,China [2]Department of Orthopaedics,The Affiliated Hospital of Southwest Medical University,Luzhou 646000,Sichuan Province,China [3]Department of Emergency,Luzhou People’s Hospital,Luzhou 646000,Sichuan Province,China

出　　处：《World Journal of Gastrointestinal Oncology》2024年第8期3624-3634,共11页世界胃肠肿瘤学杂志（英文版）（电子版）

基　　金：Supported by the Doctoral Research Initiation Fund of Affiliated Hospital of Southwest Medical University,No.21037.

摘　　要：BACKGROUND 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.AIM To explore the defensive effects of acacetin on apoptosis in H.pylori-infected GES-1 cells and to investigate the underlying mechanisms.METHODS 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.RESULTS 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.CONCLUSION 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.

关 键 词：Gastric epithelial GES-1 cells Helicobacter pylori Infection ACACETIN Antibiotic resistance APOPTOSIS 

分 类 号：R735.2[医药卫生—肿瘤]