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Alpha‐Lipoic Acid Inhibits Expression of Monocyte Chemoattractant Protein‐1 in Helicobacter pylori ‐Infected Gastric Epithelial Cells
Author(s) -
Kyung Seo Yeon,
Lim Joo Weon,
Kim Hyeyoung
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb406
Subject(s) - ampk , nadph oxidase , chemistry , helicobacter pylori , protein kinase a , reactive oxygen species , microbiology and biotechnology , western blot , kinase , biology , biochemistry , gene , genetics
Helicobacter pylori (H. pylori) causes gastritis and gastric cancers. Adenosine monophosphate‐activated protein kinase (AMPK) is a crucial regulator of energy metabolic homeostasis and a major survival factor in a variety of metabolic stresses. AMPK activation is related to anti‐inflammatory properties via inhibition of NADPH oxidase activity in various cells. Alpha‐lipoic acid (Alpha‐LA), a naturally occurring thiol compound, shows antioxidant and anti‐inflammatory effects. The aim of this study is to investigate whether alpha‐LA inhibits H. pylori ‐induced expression of pro‐inflammatory cytokine monocyte chemoattractant protein‐1 (MCP‐1) via activation of AMPK in human gastric epithelial AGS cells. Human gastric epithelial AGS cells were infected with H. pylori (strain NCTC11637) at bacterium/cell ratio of 100:1. mRNA expression of MCP‐1 were determined by real‐time PCR analysis while the levels of phospho‐AMPK and AMPK were determined by Western blot analysis. Levels of reactive oxygen species (ROS) was determined using DCF fluorescence. NADPH oxidase activity was measured by lucigenin assay. As a result, H. pylori increased NADPH oxidase activity, ROS levels and MCP‐1 expression, but decreased AMPK phosphorylation in AGS cells. Alpha‐LA inhibited H. pylori ‐induced increase in NADPH oxidase activity, MCP‐1 expression, and ROS levels in AGS cells. Alpha‐LA prevented H. pylori‐ induced decrease in AMPK phosphorylation in AGS cells. In addition, AMPK inhibitor compound C suppressed inhibitory effects of alpha‐LA on H. pylori ‐induced increase in NADPH oxidase activity, ROS production, and MCP‐1 level in AGS cells. In conclusion, alpha‐LA may inhibit MCP‐1 expression by activating AMPK and inhibiting NADPH oxidase in H. pylori ‐infected AGS cells. Consumption of alpha‐LA‐rich foods may prevent H. pylori ‐associated gastric inflammation.