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幽门螺杆菌感染的人胃窦中COX - 1、COX - 2和诱导型一氧化氮合酶蛋白的表达

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

作者信息

Franco L, Talamini G, Carra G, Doria D

机构信息

Institute of Pharmacology, University of Verona, Italy.

出版信息

Prostaglandins Other Lipid Mediat. 1999 Aug;58(1):9-17. doi: 10.1016/s0090-6980(99)00020-9.

Abstract

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 E2 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 PGE2 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 E2 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.

摘要

为了更好地理解在胃黏膜发炎情况下前列腺素和一氧化氮(NO)合成的调节机制,我们检测了9例幽门螺杆菌感染的活动性胃炎患者和6例幽门螺杆菌(HP)阴性患者胃活检组织中NO和前列腺素E2的体外生成情况,以及诱导型一氧化氮合酶(iNOS)和两种环氧化酶(COX)同工型的蛋白表达。结果表明,与未感染样本相比,HP感染患者的NO和PGE2显著增加。这些发现伴随着iNOS以及COX-1和COX-2蛋白表达的显著增加。HP阴性对照组的黏膜中未检测到iNOS和COX-2蛋白的表达。我们已经证明,iNOS蛋白在HP感染患者的胃黏膜中表达。iNOS的表达以及相应的高NO释放可能在与HP感染相关的胃炎症中起重要作用。然而,COX-1和COX-2的表达以及前列腺素E2的平行增加可能意味着这些因素可以限制黏膜损伤的程度。在先前的报道中,NO已被证明可刺激COX活性,因此我们认为NO的作用可能既在于正常功能的调节,也在于疾病的发生。

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