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Effect of Astaxanthin on Activation of Autophagy and Inhibition of Apoptosis in Helicobacter pylori -Infected Gastric Epithelial Cell Line AGS.
- Source :
-
Nutrients [Nutrients] 2020 Jun 11; Vol. 12 (6). Date of Electronic Publication: 2020 Jun 11. - Publication Year :
- 2020
-
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.
- Subjects :
- AMP-Activated Protein Kinases genetics
AMP-Activated Protein Kinases metabolism
Anti-Inflammatory Agents
Antioxidants
Apoptosis genetics
Autophagy genetics
Cell Line, Tumor
Gastric Mucosa cytology
Humans
Microtubule-Associated Proteins genetics
Microtubule-Associated Proteins metabolism
Phosphorylation drug effects
Signal Transduction drug effects
Signal Transduction genetics
TOR Serine-Threonine Kinases genetics
TOR Serine-Threonine Kinases metabolism
Xanthophylls pharmacology
Antineoplastic Agents
Apoptosis drug effects
Autophagy drug effects
Epithelial Cells microbiology
Epithelial Cells physiology
Gastritis microbiology
Gastritis physiopathology
Helicobacter Infections
Helicobacter pylori
Subjects
Details
- Language :
- English
- ISSN :
- 2072-6643
- Volume :
- 12
- Issue :
- 6
- Database :
- MEDLINE
- Journal :
- Nutrients
- Publication Type :
- Academic Journal
- Accession number :
- 32545395
- Full Text :
- https://doi.org/10.3390/nu12061750