Effect of astaxanthin on activation of autophagy and inhibition of apoptosis in Helicobacter pylori‐ infected gastric epithelial cell line AGS

Hanbit Lee, Joo Weon Lim, Hyeyoung Kim

Research output: Contribution to journalArticlepeer-review

21 Citations (Scopus)

Abstract

Helicobacter pylori (H. pylori) infection leads to the massive apoptosis of the gastric epithelial cells, causing gastric ulcers, gastritis, and gastric adenocarcinoma. Autophagy is a cellular recycling process that plays important roles in cell death decisions and can protect cells by preventing apoptosis. Upon the induction of autophagy, the level of the autophagy substrate p62 is reduced and the autophagy‐related ratio of microtubule‐associated proteins 1A/1B light chain 3B (LC3B)‐II/LC3B‐I is heightened. AMP‐activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) are involved in the regulation of autophagy. Astaxanthin (AST) is a potent anti-oxidant that plays anti‐inflammatory and anti‐cancer roles in various cells. In the present study, we examined whether AST inhibits H. pylori‐induced apoptosis through AMPK‐mediated autophagy in the human gastric epithelial cell line AGS (adenocarcinoma gastric) in vitro. In this study, H. pylori induced apoptosis. Compound C, an AMPK inhibitor, enhanced the H. pylori‐induced apoptosis of AGS cells. In contrast, metformin, an AMPK activator, suppressed H. pylori‐induced apoptosis, showing that AMPK activation inhibits H. pylori‐induced apoptosis. AST inhibited H. pylori‐induced apoptosis by increasing the phosphorylation of AMPK and decreasing the phosphorylation of RAC-alpha serine/threonine‐protein kinase (Akt) and mTOR in H. pylori‐stimulated cells. The number of LC3B puncta in H. pylori‐stimulated cells increased with AST. These results suggest that AST suppresses the H. pylori‐induced apoptosis of AGS cells by inducing autophagy through the activation of AMPK and the downregulation of its downstream target, mTOR. In conclusion, AST may inhibit gastric diseases associated with H. pylori infection by increasing autophagy through the activation of the AMPK pathway.

Original languageEnglish
Article number1750
Pages (from-to)1-18
Number of pages18
JournalNutrients
Volume12
Issue number6
DOIs
Publication statusPublished - 2020 Jun

Bibliographical note

Funding Information:
Funding: This study was supported financially by a grant from the National Research Foundation (NRF) of Korea, which is funded by the Korean Government (NRF‐2018R1A2B2005575).

Publisher Copyright:
© 2020 by the authors.

All Science Journal Classification (ASJC) codes

  • Food Science
  • Nutrition and Dietetics

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