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Exogenous hydrogen sulfide attenuates gastric ischemia-reperfusion injury via activation of KATP channel
Author(s): 
Pages: 27-32
Year: Issue:  1
Journal: Acta Physiologica Sinica

Keyword:  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;
Abstract: 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30min再灌注1h,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14d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。
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