Expression of COX-1, COX-2, and inducible nitric oxide synthase protein in human gastric antrum with Helicobacter pylori infection

被引:37
作者
Franco, L [1 ]
Talamini, G
Carra, G
Doria, D
机构
[1] Univ Verona, Policlin Borgo Roma, Inst Pharmacol, I-37134 Verona, Italy
[2] Univ Verona, Policlin Borgo Roma, Gastroenterol Unit, I-37134 Verona, Italy
[3] Univ Verona, Inst Biol Chem, I-37100 Verona, Italy
来源
PROSTAGLANDINS & OTHER LIPID MEDIATORS | 1999年 / 58卷 / 01期
关键词
nitric oxide; prostaglandin E-2; Helicobacter pylori; cyclo-oxygenase;
D O I
10.1016/S0090-6980(99)00020-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
For a better understanding of the regulation of prostaglandin and nitric oxide (NO) synthesis in circumstances in which the gastric mucosa is inflamed, we have examined the ex vivo production of NO and prostaglandin E-2 and the protein expression of inducible nitric oxide synthase (iNOS) and 2 cyclo-oxygenase (COX) isoforms in gastric biopsies from nine Helicobacter pylori-infected patients with active gastritis and six Helicobacter pylori (HP)-negative patients. The results indicate a significant increased of NO and PGE(2) in patients with HP infection compared with uninfected samples. These findings were paralleled by marked increases in iNOS and in COX-1 and COX-2 protein expression. Expression of iNOS and COX-2 protein was absent in the mucosa of HP-negative controls. We have demonstrated that iNOS protein is expressed in the gastric mucosa of patients with HP infection. It is likely that iNOS expression and the corresponding high release of NO may play an important role in gastric inflammation associated with HP infection. However, the expression of COX-1 and COX-2 and the parallel increase of prostaglandin E-2 could imply that these factors could limit the extend of mucosal damage. In previous reports NO has been shown to stimulate the COX activity, so we think that the role of NO could be both in the regulation of normal function and in the genesis of diseases. (C) 1999 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:9 / 17
页数:9
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