Helicobacter pylori에 감염된 AGS 세포에서 IL-8 발현에 대한 산화감지 전사인자의 역할

Abstract

Background/Aims: Oxygen radicals are important regulators in Helicobacter pylori (H. pylori)-induced gastric ulceration and carcinogenesis. IL-8 may be regulated by oxidant-sensitive transcription factors, nuclear-κB (NF-κB), and activator protein-1 (AP-1). The present study aims to investigate whether H. pylori-induced IL-8 expression is regulated by NF-κB and AP-1 in gastric epithelial AGS cells and whether this transcriptional regulation of IL-8 is inhibited by N-acetylcysteine (NAC). Methods: H. pylori was added to the cell at a bacterium/cell ratio of 500：1 in the presence or absence of NAC (1, 5, 10 mM) mRNA expression and protein level was determined by Northern blot analysis and enzyme-linked immunosorbent assay (ELISA), respectively. DNA binding activities of NF-κB and AP-1 were investigated by electrophoretic mobility shift assay (EMSA) and degradation of IκBα protein was monitored by western blot analysis. Results: H. pylori induced the expression of mRNA and protein for IL-8 via activation of NF-κB and AP-1. NF-κB activation accompanied by a decrease in I-κBα in H. pylori-infected AGS cells. NAC inhibited H. pylori-induced activation of transcription factors and IL-8 expression in AGS cells. Conclusions: oxygen radicals induce the activation of NF-κB and AP-1 and IL-8 expression. Antioxidants such as NAC might be useful anti-inflammatory agents by inhibiting activation of transcription factors and decreasing IL-8 production in H. pylori-induced gastric inflammation.