Experimental study on Helicobacter pylori-related gastric carcinogenesis mediated by interleukin-1β
- VernacularTitle:白细胞介素-1β介导幽门螺杆菌相关胃癌发生的实验研究
- Author:
Tao GUO
;
Jiaming QIAN
;
Yuqing ZHAO
;
Xiaobo LI
;
Jianzhong ZHANG
- Publication Type:Journal Article
- Keywords:
Stomach neoplasms;
Interleukin-1;
Helicobacter pylori
- From:
Chinese Journal of Digestion
2008;28(4):217-220
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the potential mechanism of interleukin-1β(IL-1β)in H.pylori-related gastric carcinogenesis.Methods Human gastric cancer cell line(AGS),human gastric epithelial cell line(GES-1)and isolated parietal cells were treated with exogenous IL-1β(10 ng/ml)in the presence or absence of H.pylori(NCTC 11637).Cell proliferation and apoptosis were determined by MTT assay and flow cytometry,respectively. Expressions of cyclooxygenase-2(COX-2)mRNA and protein were examined using RT-PCR and flow cytometry,respectively.Acid secretion by parietal cells was tested using 14C-aminopyrine(14 C-AP) accumulation indirectly.H+/K+ ATPase α subunit mRNA expression was assessed using RT-PCR.Results The cell proliferation and H.pylori-related apoptosis in both GES-1 and AGS celL lines were stimulated and inhibited by IL-1β.IL-1β induced expression and upregulation of COX-2 mRNA in GES-1 and AGS cell lines,respectively.In addition,IL-1β continuously inhibited the ability of histamine-stimulated 14C-AP accumulation of isolated parietal cells accompanied by down-regulation of H+/K+ ATPase mRNA expression.Conclusions It suggests that IL-1β play an important role in H.pylori-related gastric carcinogenesis through two pathways:①to interfere gastric epithelial cell growth by up-regulating COX-2 expression,②to inhibit acid secretion from parietal cell by down-regulating H+/K+ ATPase expression.
