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[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

Received: 2011-08-10　　Accepted: 2011-11-14

Corresponding author: 闫长栋　　E-mail: yancd55@163.com

Citing This Article：

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).