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Astaxanthin Inhibits Matrix Metalloproteinase Expression by Suppressing PI3K/AKT/mTOR Activation in Helicobacter

Jimin Lee1, Joo Weon Lim1, Hyeyoung Kim1

  • 1Department of Food and Nutrition, BK21 FOUR, College of Human Ecology, Yonsei University, Seoul 03722, Korea.

Nutrients
|August 26, 2022
PubMed

Insights

Astaxanthin, an antioxidant, inhibits Helicobacter pylori (H. pylori)-induced gastric cell invasion and migration. It suppresses matrix metalloproteinase (MMP) expression by blocking the PI3K/AKT/mTOR/NF-κB signaling pathway.

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Cancer Research

Background:

  • Helicobacter pylori (H. pylori) infection elevates reactive oxygen species (ROS) and activates signaling pathways, including mitogen-activated protein kinase (MAPK), leading to matrix metalloproteinase (MMP) expression and gastric cell invasion.
  • The PI3K/AKT/mTOR signaling pathway is implicated in MMP expression and cancer progression, and ROS can activate this pathway in cancer cells.

Purpose of the Study:

  • To investigate the effect of astaxanthin on H. pylori-induced MMP expression, cell invasion, and migration in gastric epithelial cells.
  • To determine if astaxanthin inhibits the PI3K/AKT/mTOR signaling pathway in H. pylori-infected gastric cells.

Main Methods:

  • Gastric epithelial AGS cells were infected with H. pylori, and the effects of astaxanthin treatment were analyzed.
  • Key signaling molecules (PI3K, AKT, mTOR, NF-κB, IκBα) and MMP expression (MMP-7, MMP-10) were assessed.
  • Cell invasion and migration assays were performed.

Main Results:

  • H. pylori infection activated PI3K/AKT/mTOR and NF-κB signaling, decreased IκBα, and increased MMP-7, MMP-10 expression, cell invasion, and migration.
  • Astaxanthin treatment suppressed these H. pylori-induced changes.
  • Specific inhibitors of PI3K, AKT, and mTOR reversed H. pylori-stimulated NF-κB activation and IκBα reduction.

Conclusions:

  • Astaxanthin effectively inhibits H. pylori-induced MMP expression, gastric cell invasion, and migration.
  • The mechanism involves the suppression of the PI3K/AKT/mTOR/NF-κB signaling pathway.
Keywords:
Helicobacter pyloriastaxanthingastric epithelial cellsmammalian target of rapamycinmetalloproteinasephosphatidylinositol 3-kinaseserine/threonine protein kinase B

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