【摘要】 目的 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。方法 雄性Sprague-Dawley（SD）大鼠，实验分3组：假手术（Sham）组、GI-R组和NaHS组。采用夹闭腹腔动脉30 min再灌注1 h方法建立GI-R损伤模型。GI-R后处死各组大鼠，采用Adobe Photoshop软件分析计算GI-R引起的胃黏膜损伤面积，苏木精-伊红染色后光镜下观察GI-R引起的胃黏膜损伤深度，化学比色法检测大鼠胃黏膜中过氧化氢（H₂O₂）和谷胱甘肽（GSH）含量，免疫印迹法测定大鼠胃黏膜组织中Keap1、Nrf2、超氧化物歧化酶（SOD2）和黄嘌呤氧化酶（XOD）的表达，免疫组化法检测大鼠胃黏膜Keap1和Nrf2表达。结果 GI-R组胃黏膜损伤明显、损伤深度较深，NaHS组胃黏膜损伤面积和深度较GI-R组明显缩小和减少。与GI-R组相比，NaHS预处理后能增加胃黏膜组织中GSH、Nrf2、SOD2水平（P<0.05）,降低H₂O₂、Keap1、XOD水平（P<0.05）。结论 外源性H₂S预处理可以通过Keap1-Nrf2信号通路减轻大鼠胃缺血再灌注引起的黏膜损伤。更多还原

【Abstract】 Objective To investigate the protective effects of exogenous hydrogen sulfide donor NaHS pre-treatment on gastric mucosal injury induced by gastric ischemia-reperfusion（GI-R） in rats and possible mechanisms. Methods Male SD rats were randomly divided into a sham operation group, a GI-R group and a NaHS treatment group. A GI-R model was induced by clamping the celiac artery of these rats for 30 min followed by reperfusion for 1 h. These rates were sacrificed and the areas of their gastric mucosal injury was analyzed using Adobe Photoshop software. The depth of the injury was measured under a light microscopy after Hematoxylin-Eosin staining. The amounts of H₂O₂ and GSH in the gastric mucosal were determined by colorimetric method. The levels of Keap1, Nrf2, superoxide dismutase（SOD2） and xanthine oxidase（XOD） in the gastric mucosal were examined by immunohistochemical method. Results Obvious gastric mucosal injury was seen in the GI-R group. In contrast, the rats in the NaHS group produced remarkably smaller areas of the injury. Compared with the GI-R group, the NaHS pre-treatment group presented increased amounts of GSH, Nrf2 and SOD2, while their levels of H₂O₂, Keap1 and XOD were reduced（P<0.05）. Conclusion Exogenous hydrogen sulfide can play a protective role against GI-R injury in rats through activation of the Keap1-Nrf2 pathway.更多还原