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外源性H2S通过激活KATP通道减轻大鼠胃缺血再灌注引起的胃黏膜损伤

邹吉贺, 乔伟丽, 王光明, 马鸿基, 祁友键, 孙红, 闫长栋^*

徐州医学院 生理学教研室；神经生物学实验室，徐州 221002

摘要

本文旨在观察外源性硫化氢(hydrogen sulfide, H2S)供体NaHS预处理对大鼠胃缺血再灌注(gastric ischemia-reperfusion, GI-R)损伤的影响及其可能的作用机制。实验分5组：假手术(sham)组、GI-R组、NaHS组、格列苯脲(glibenclamide)组和吡那地尔(pinacidil)组。采用夹闭雄性Sprague-Dawley (SD)大鼠腹腔动脉30 min再灌注1 h，建立GI-R损伤模型。采用Adobe Photoshop软件分析计算GI-R引起的胃黏膜损伤面积，利用HE染色分析GI-R引起的胃黏膜损伤深度，通过比色法测定血浆中H2S的含量。结果显示，与假手术(sham)组相比，GI-R组胃黏膜损伤面积和损伤深度明显增加；NaHS预处理能够显著减小GI-R引起的胃黏膜损伤面积和损伤深度；但是NaHS预处理14 d对血浆中的H2S浓度没有显著的影响。与NaHS预处理组相比，GI-R前给予ATP敏感K+通道(KATP)阻断剂格列苯脲和NaHS预处理，加重GI-R引起的胃黏膜损伤程度；与GI-R组相比，单独给予KATP通道开放剂吡那地尔能够抑制GI-R的损伤作用，保护胃黏膜。上述结果提示，外源性H2S通过开放KATP通道减轻GI-R引起的胃黏膜损伤，起到保护胃黏膜的作用。

关键词： 硫化氢; 胃缺血再灌注; ATP敏感K+通道; 预处理; 胃黏膜细胞; 大鼠

分类号：R333.2

[Exogenous hydrogen sulfide attenuates gastric ischemia-reperfusion injury via activation of K(ATP) channel.] [Article in Chinese]

ZOU Ji-He, QIAO Wei-Li, WANG Guang-Ming, MA Hong-Ji, QI You-Jian, SUN Hong, YAN Chang-Dong^*

Department of Physiology； Laboratory of Neurobiology, Xuzhou Medical College, Xuzhou 221002, China

Abstract

The present study aimed to investigate the protective effect and mechanism of hydrogen sulfide donor NaHS administration against gastric mucosal injury induced by gastric ischemia-reperfusion (GI-R) in rats. GI-R injury was induced by clamping the celiac artery of adult male SD rats for 30 min and followed by reperfusion for 1 h. The rats were randomly divided into sham group, GI-R group, NaHS group, glibenclamide group and pinacidil group. Gastric mucosal damage was analyzed with macroscopic injured area, deep damage was assessed with histopathology scores, and the hydrogen sulfide concentration in plasma was determined by colorimetric method. The results showed that pretreatment of NaHS significantly reduced the injured area and deep damage of the gastric mucosa induced by GI-R. However, NaHS did not significantly alter the levels of hydrogen sulfide in plasma 14 d after NaHS administration. The gastric protective effect of NaHS during reperfusion could be attenuated by glibenclamide, an ATP-sensitive potassium channel (KATP) blocker. However, KATP opener pinacidil inhibited the GI-R-induced injury. These results suggest that exogenous hydrogen sulfide plays a protective role against GI-R injury in rats possibly through modulation of KATP channel opening.

Key words: hydrogen sulfide; gastric ischemia-reperfusion; ATP-sensitive potassium channel; preconditioning; gastric mucosal cell; rat

收稿日期：2011-08-10　　录用日期：2011-11-14

通讯作者：闫长栋　　E-mail: yancd55@163.com

引用本文：

邹吉贺, 乔伟丽, 王光明, 马鸿基, 祁友键, 孙红, 闫长栋. 外源性H2S通过激活KATP通道减轻大鼠胃缺血再灌注引起的胃黏膜损伤[J]. 生理学报 2012; 64 (1): 27-32.

ZOU Ji-He, QIAO Wei-Li, WANG Guang-Ming, MA Hong-Ji, QI You-Jian, SUN Hong, YAN Chang-Dong. [Exogenous hydrogen sulfide attenuates gastric ischemia-reperfusion injury via activation of K(ATP) channel.] [Article in Chinese]. Acta Physiol Sin 2012; 64 (1): 27-32 (in Chinese with English abstract).