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克罗恩病和溃疡性结肠炎患者血清中的血管紧张素I转换酶和羧肽酶N

Serum angiotensin-I-converting enzyme and carboxypeptidase N in Crohn's disease and ulcerative colitis.

作者信息

Sommer H, Schweisfurth H, Schulz M

出版信息

Enzyme. 1986;35(4):181-8. doi: 10.1159/000469341.

Abstract

Angiotensin-I-converting enzyme (ACE) and carboxypeptidase N1 and N2 (CPN1, CPN2) inactivate kinins and might therefore play a role in the development of inflammatory reactions via an influence on the release of prostaglandins and inactivation of anaphylatoxic peptides of the complement system. In the present study, the serum activity of these enzymes was determined in 60 patients with Crohn's disease, 18 patients with ulcerative colitis and 70 healthy control subjects. ACE was significantly lowered in active Crohn's disease (CDAI greater than 150) and in ulcerative colitis (p less than 0.01), as long as the ileum or cecum was affected. Since ACE was detected in high concentrations in the human intestinal mucosa, decreased values may be explained by damage to the site of its production. CPN1 and CPN2 were raised in both diseases (p less than 0.005), irrespective of their activity and location. These alterations in the activity of the kininases investigated may play a role in the pathogenesis of inflammatory bowel diseases.

摘要

血管紧张素转换酶(ACE)以及羧肽酶N1和N2(CPN1、CPN2)可使激肽失活,因此可能通过影响前列腺素的释放以及补体系统过敏毒素肽的失活,在炎症反应的发生发展中发挥作用。在本研究中,对60例克罗恩病患者、18例溃疡性结肠炎患者以及70名健康对照者测定了这些酶的血清活性。只要回肠或盲肠受到影响,活动期克罗恩病(CDAI大于150)和溃疡性结肠炎患者的ACE显著降低(p小于0.01)。由于在人肠黏膜中检测到高浓度的ACE,其数值降低可能是由于其产生部位受损所致。CPN1和CPN2在这两种疾病中均升高(p小于0.005),与疾病的活动度和部位无关。所研究的激肽酶活性的这些改变可能在炎症性肠病的发病机制中起作用。

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