Article Publish Status: FREE
Abstract Title:

Effect of Astaxanthin on Activation of Autophagy and Inhibition of Apoptosis in-Infected Gastric Epithelial Cell Line AGS.

Abstract Source:

Nutrients. 2020 Jun 11 ;12(6). Epub 2020 Jun 11. PMID: 32545395

Abstract Author(s):

Hanbit Lee, Joo Weon Lim, Hyeyoung Kim

Article Affiliation:

Hanbit Lee


() 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-induced apoptosis through AMPK-mediated autophagy in the human gastric epithelial cell line AGS (adenocarcinoma gastric) in vitro. In this study,induced apoptosis. Compound C, an AMPK inhibitor, enhanced the-induced apoptosis of AGS cells. In contrast, metformin, an AMPK activator, suppressed-induced apoptosis, showing that AMPK activation inhibits-induced apoptosis. AST inhibited-induced apoptosis by increasing the phosphorylation of AMPK and decreasing the phosphorylation of RAC-alpha serine/threonine-protein kinase (Akt) and mTOR in-stimulated cells. The number of LC3B puncta in-stimulated cells increased with AST. These results suggest that AST suppresses the-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 withinfection by increasing autophagy through the activation of the AMPK pathway.

Study Type : In Vitro Study

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Sayer Ji
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