{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T07:25:59Z","timestamp":1784186759494,"version":"3.55.0"},"reference-count":49,"publisher":"Baishideng Publishing Group Inc.","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["World J Gastrointest Oncol"],"abstract":"<jats:p>BACKGROUND<\/jats:p>\n          <jats:p>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.<\/jats:p>\n          <jats:p>AIM<\/jats:p>\n          <jats:p>To explore the defensive effects of acacetin on apoptosis in H. pylori -infected GES-1 cells and to investigate the underlying mechanisms.<\/jats:p>\n          <jats:p>METHODS<\/jats:p>\n          <jats:p>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.<\/jats:p>\n          <jats:p>RESULTS<\/jats:p>\n          <jats:p>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.<\/jats:p>\n          <jats:p>CONCLUSION<\/jats:p>\n          <jats:p>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.<\/jats:p>","DOI":"10.4251\/wjgo.v16.i8.3624","type":"journal-article","created":{"date-parts":[[2024,8,7]],"date-time":"2024-08-07T01:46:11Z","timestamp":1722995171000},"page":"3624-3634","source":"Crossref","is-referenced-by-count":7,"title":["Effect of acacetin on inhibition of apoptosis in <i>Helicobacter pylori<\/i>-infected gastric epithelial cell 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