Cho S O, Kim K H, Kim H
Department of Pharmacology and Institute of Gastroenterology, Brain Korea 21 Project for Medical Sciences, College of Medicine Yonsei University, Seoul, 20-52, Korea.
Inflammopharmacology. 2007 Feb;15(1):26-30. doi: 10.1007/s10787-006-1547-z.
In Helicobacter pylori (H. pylori)-induced gastric ulceration, NF-kappaB regulates the expression of inflammatory genes. NF-kappaB is activated by phosphorylation of its endogenous inhibitor, IkappaBalpha. The possible involvement of mitogen-activated protein kinase (MAPK) on NF-kappaB activation has been suggested in various cells. Present study aims to investigate whether H. pylori in a Korean isolate induces phosphorylation of IkappaBalpha and whether H. pylori-induced phosphorylation of IkappaBalpha is mediated by MAPK in gastric epithelial AGS cells. AGS cells were treated with MAPK inhibitors (U0126 for extracellular signal-regulated kinase, SB203580 for p38 kinase, SP600125 for c-Jun NH2-terminal protein kinases) and stimulated with H. pylori. As a result, H. pylori increased phospho-specific IkappaBalpha accompanied with the decrease in control IkappaBalpha. H. pylori-induced phosphorylation of IkappaBalpha was inhibited by treatment of U0126, but not by SB203580 or SP600125. In conclusion, extracellular signal-regulated kinase induces phosphorylation of IkappaBalpha in H. pylori-infected AGS cells.
在幽门螺杆菌（H. pylori）诱导的胃溃疡中，核因子-κB（NF-κB）调节炎症基因的表达。NF-κB通过其内源性抑制剂IκBα的磷酸化而被激活。在各种细胞中，有研究提示丝裂原活化蛋白激酶（MAPK）可能参与NF-κB的激活。本研究旨在探讨一株韩国分离的幽门螺杆菌是否诱导IκBα磷酸化，以及幽门螺杆菌诱导的IκBα磷酸化是否由胃上皮AGS细胞中的MAPK介导。用MAPK抑制剂（U0126用于细胞外信号调节激酶，SB203580用于p38激酶，SP600125用于c-Jun氨基末端蛋白激酶）处理AGS细胞，并用幽门螺杆菌刺激。结果显示，幽门螺杆菌使磷酸化特异性IκBα增加，同时对照IκBα减少。U0126处理可抑制幽门螺杆菌诱导的IκBα磷酸化，但SB203580或SP600125处理则无此作用。总之，细胞外信号调节激酶在幽门螺杆菌感染的AGS细胞中诱导IκBα磷酸化。
