Basic Study
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Aug 15, 2024; 16(8): 3624-3634
Published online Aug 15, 2024. doi: 10.4251/wjgo.v16.i8.3624
Effect of acacetin on inhibition of apoptosis in Helicobacter pylori-infected gastric epithelial cell line
Qi-Xi Yao, Zi-Yu Li, Hou-Le Kang, Xin He, Min Kang
Qi-Xi Yao, Xin He, Min Kang, Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan Province, China
Zi-Yu Li, Department of Orthopaedics, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan Province, China
Hou-Le Kang, Department of Emergency, Luzhou People’s Hospital, Luzhou 646000, Sichuan Province, China
Co-first authors: Qi-Xi Yao and Zi-Yu Li.
Author contributions: Yao QX conducted the relevant experiments; Li ZY assisted in the completion of the experiments; Yao QX and Li ZY wrote the manuscript and revised and approved the final version; Kang HL and He X collected and analyzed the data; Kang M designed the research and made critical revisions to the manuscript. Yao QX and Li ZY contributed equally to this study, and all authors have read and approved the final version of the article.
Supported by the Doctoral Research Initiation Fund of Affiliated Hospital of Southwest Medical University, No. 21037.
Institutional review board statement: The study was reviewed and approved by the Affiliated Hospital of Southwest Medical University Institutional Review Board (Approval No. KY2024192).
Conflict-of-interest statement: The authors declare that they have no competing interests.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Min Kang, MD, PhD, Associate Chief Physician, Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, No. 25 Taiping Street, Luzhou 646000, Sichuan Province, China. 598385140@qq.com
Received: April 9, 2024
Revised: May 15, 2024
Accepted: May 31, 2024
Published online: August 15, 2024
Processing time: 120 Days and 23.4 Hours
Abstract
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.

Keywords: Gastric epithelial GES-1 cells, Helicobacter pylori, Infection, Acacetin, Antibiotic resistance, Apoptosis

Core Tip: Helicobacter pylori (H. pylori), a common human microaerophilic gram-negative rod, is crucial in the progression of chronic gastritis, gastrointestinal metaplasia, and gastric atypical hyperplasia to gastric cancer. We have examined the protective role of acacetin against apoptosis in H. pylori-infected GES-1 cells. However, the role of acacetin in the apoptosis of gastric epithelial cells induced by H. pylori infection has not been previously reported. Therefore, this study offers a new perspective for early intervention in H. pylori-induced chronic gastritis and may provide synergistic effects and novel therapeutic directions for the clinical eradication of H. pylori in conjunction with the standard quadruple therapy.