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大鼠肠道中一氧化氮合酶的诱导及其与组织损伤的关联。

Induction of nitric oxide synthase in rat intestine and its association with tissue injury.

作者信息

Boughton-Smith N K, Evans S M, Whittle B J, Moncada S

机构信息

Department of Pharmacology, Wellcome Research Laboratories, Beckenham, Kent, UK.

出版信息

Agents Actions. 1993;38 Spec No:C125-6. doi: 10.1007/BF01991159.

Abstract

Induction of a calcium-independent nitric oxide synthase (NOS) has been detected in the rat small intestine and colon, 3-5 h following endotoxin (3 mg kg-1 i.v.). This was associated with an increase in vascular permeability to plasma protein in jejunum and colon, and both induction of NOS and vascular leakage were inhibited by pretreatment with dexamethasone (1 mg kg-1 s.c.). Induction of colonic NOS was also detected in a TNB colitis model, 24 h after challenge. Thus, increased NO synthesis may be involved in the microvascular and mucosal injury associated with inflammatory diseases of the gut.

摘要

在内毒素(3毫克/千克静脉注射)后3至5小时,已在大鼠小肠和结肠中检测到钙非依赖性一氧化氮合酶(NOS)的诱导。这与空肠和结肠中血浆蛋白的血管通透性增加有关,并且NOS的诱导和血管渗漏均被地塞米松(1毫克/千克皮下注射)预处理所抑制。在TNB结肠炎模型中,攻击后24小时也检测到结肠NOS的诱导。因此,增加的NO合成可能参与了与肠道炎症性疾病相关的微血管和粘膜损伤。

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