外源性硫化氢通过Keapl—Nrf2信号通路减轻胃缺血再灌注引起的黏膜损伤  

Exogenous hydrogen sulfide attenuates gastric ischemia- reperfusion injury via the Keapl -Nrf2 pathway

作　　者：吴迪[1] 刘磊[1] 王光明[1] 石玥[1] 闫长栋[1] 

机构地区：[1]徐州医学院生理学教研室,江苏徐州221004

出　　处：《徐州医学院学报》2015年第1期28-32,共5页Acta Academiae Medicinae Xuzhou

基　　金：国家自然科学基金（81200250）;江苏省自然科学基金（BK20131119）;徐州医学院研究生培养创新工程课题（xyyCB-14）

摘　　要：目的观察外源性硫化氢（hydrogensulfide，H：S）供体NariS预处理对大鼠胃缺血再灌注（gastricische—mia—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30min再灌注1h方法建立GI—R损伤模型。GI～R后处死各组大鼠，采用AdobePhotoshop软件分析计算GI～R引起的胃黏膜损伤面积，苏木精一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Keapl、Nrt2、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Keapl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、Keapl、XOD水平（P〈0．05）。结论外源性Hs预处理可以通过Keapl—Nrf2信号通路减轻大鼠胃缺血再灌注引起的黏膜损伤。Objective To investigate the protective effects of exogenous hydrogen sulfide donor NariS 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 NariS 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 Keapl, 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 NariS group produced remarkably smaller areas of the injury. Compared with the GI - R group, the NariS pre - treatment group presented increased amounts of GSH, Nrf2 and SOD2, while their levels of H2O2, Keapl 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 Keapl - Nrf2 pathway.

关 键 词：硫化氢 胃缺血再灌注 KEAP1 NRF2 

分 类 号：R333.2[医药卫生—人体生理学]