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KMID : 0311120160570010260
Yonsei Medical Journal
2016 Volume.57 No. 1 p.260 ~ p.264
¥á-Lipoic Acid Inhibits Expression of IL-8 by Suppressing Activation of MAPK, Jak/Stat, and NF-¥êB in H. pylori-Infected Gastric Epithelial AGS Cells
Choi Ji-Hyun

Cho Soon-Ok
Kim Hye-Young
Abstract
The epithelial cytokine response, associated with reactive oxygen species (ROS), is important in Helicobacter pylori (H. pylori)-induced inflammation. H. pylori induces the production of ROS, which may be involved in the activation of mitogen-activated protein kinases (MAPK), janus kinase/signal transducers and activators of transcription (Jak/Stat), and oxidant-sensitive transcription factor, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-¥êB), and thus, expression of interleukin-8 (IL-8) in gastric epithelial cells. ¥á-lipoic acid, a naturally occurring thiol compound, is a potential antioxidant. It shows beneficial effects in treatment of oxidant-associated diseases including diabetes. The present study is purposed to investigate whether ¥á-lipoic acid inhibits expression of inflammatory cytokine IL-8 by suppressing activation of MAPK, Jak/Stat, and NF-¥êB in H. pylori-infected gastric epithelial cells. Gastric epithelial AGS cells were pretreated with or without ¥á-lipoic acid for 2 h and infected with H. pylori in a Korean isolate (HP99) at a ratio of 300:1. IL-8 mRNA expression was analyzed by RT-PCR analysis. IL-8 levels in the medium were determined by enzyme-linked immunosorbent assay. NF-¥êB-DNA binding activity was determined by electrophoretic mobility shift assay. Phospho-specific and total forms of MAPK and Jak/Stat were assessed by Western blot analysis. ROS levels were determined using dichlorofluorescein fluorescence. As a result, H. pylori induced increases in ROS levels, mRNA, and protein levels of IL-8, as well as the activation of MAPK [extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun NH2-terminal kinase 1/2 (JNK1/2), p38], Jak/Stat (Jak1/2, Stat3), and NF-¥êB in AGS cells, which was inhibited by ¥á-lipoic acid. In conclusion, ¥á-lipoic acid may be beneficial for prevention and/or treatment of H. pylori infection-associated gastric inflammation.
KEYWORD
¥á-lipoic acid, Helicobacter pylori, IL-8, NF-¥êB, MAPK, Jak/Stat
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