Role of NF-kappaB and AP-1 on Helicobater pylori-induced IL-8 expression in AGS cells.
Study Design
- Тип исследования
- In Vitro
- Популяция
- Human gastric epithelial cells
- Вмешательство
- Role of NF-kappaB and AP-1 on Helicobater pylori-induced IL-8 expression in AGS cells. None
- Препарат сравнения
- None
- Первичный исход
- NF-kappaB/AP-1 role in H. pylori IL-8 expression
- Направление эффекта
- Mixed
- Риск систематической ошибки
- Unclear
Abstract
Oxygen radicals are important regulators in Helicobacter pylori-induced gastric ulceration and carcinogenesis. IL-8 may be regulated by oxidant-sensitive transcription factors, NF-kappaB, and AP-1. The present study aims to investigate whether H. pylori-induced IL-8 expression is regulated by NF-kappaB and AP-1 in gastric epithelial AGS cells and whether this transcriptional regulation of IL-8 is inhibited by N-acetylcysteine (NAC). As a result, H. pylori induced the expression of mRNA and protein for IL-8 via activation of NF-kappaB and AP-1. NF-kappaB activation accompanied by a decrease in I-kappaBalpha and activated AP-1 complex was a c-jun/c-fos heterodimer in H. pylori-infected AGS cells. NAC inhibited H. pylori-induced activation of transcription factors and IL-8 expression in AGS cells. In conclusion, oxygen radicals induce the activation of NF-kappaB 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.
Кратко
In conclusion, oxygen radicals induce the activation of NF-κB and AP-1 and IL-8 expression andAntioxidants such as NAC might be useful anti-inflammatory agents by inhibiting activation of transcription factors and decreasingIL-8 production in H. pylori-induced gastric inflammation.
Used In Evidence Reviews
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