硫化氢预处理延迟相对大鼠心肌缺血再灌注时谷胱甘肽S转移酶表达的影响

Effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase expression during myocardial ischemia-reperfusion in rats

目的:探讨硫化氢预处理延迟相对大鼠心肌缺血再灌注时谷胱甘肽S转移酶表达的影响。方法:健康成年Sprague-Dawley雄性大鼠40只,随机分成4组:假手术组(S组)仅开胸、分离冠状动脉左前降支,不阻断血流150 min;缺血再灌注组(IR组)行冠状动脉左前降支阻断30 min,再灌注120 min;硫化氢预处理延迟相组(H组)静脉注射硫化氢(0.05 mg/kg),给药后24 h同IR组处理;硫化氢预处理延迟相+线粒体KATP通道阻断剂(5-羟葵酸,5-HD)组(D组)缺血前15min静脉注射5-HD 5 mg/kg,其它同H组处理。再灌注结束后测心肌谷胱甘肽S转移酶(GST)的表达和心梗面积,观察心肌细胞超微结构。结果:与IR组(38.27±5.64)%比,H组(25.40±3.54)%心肌梗死面积减小(P<0.05),D组(40.53±5.24)%无明显差异(P>0.05)。与S组比,IR组、H组和D组GST均升高(P<0.05),与IR组比,H组GST增高(P<0.05),D组无明显差异(P>0.05)。与IR组比,电镜下H组心肌细胞损伤程度减轻,D组无明显差异。结论:硫化氢预处理延迟相对大鼠心肌的保护作用可能与上调心肌谷胱甘肽S转移酶表达有关。

Objective: To investigate the effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase(GST) expression during myocardial ischemia-reperfusion in rats. Methods: Sprague-Dawley male rats were randomly divided into 4 groups(n= 10 in each):Group S(sham operation group),Group IR(ischemia/reperfusion group),Group H(IR+ NaHS 0.05 mg/kg iv,24 h before ischemia) and Groups D receiving IR+NaHS 24 h before ischemia and 5-hydroxydecanoate(5-HD) 15 min before ischemia.Animals in groups IR,H and D were subjected to ischemia by 30 min of coronary artery occlusion followed by 2 h of reperfusion.At the end of the reperfusion,myocardial infarct size(IS) was examined.Glutathione S-transferase(GST) was measured by Western blotting.The myocardial ultrastructures were observed under the electron microscopy. Results: The IS was significantly smaller in Group H than that in Group IR [(25.40±3.54)% vs(38.27±5.64)%,P<0.05].The GST expression in myocardium was significantly higher in Group H than that in Group IR.Microscopic examination showed less myocardial damage in Group H than in Group IR.The protective effects of delayed preconditioning by hydrogen sulfide was prevented by 5-HD pretreatrnent. Conclusion: The hydrogen sulfide-induced delayed preconditioning attenuates myocardial IR injury possibly through up-regulating glutathione S-transferase expression in rats.