羟基红花黄色素A对心肌缺血再灌注损伤的作用及其机制的探讨

目的:探讨羟基红花黄色素A(HSYA)是否能够保护心脏的再灌注损伤及其作用机制。方法:采用离体大鼠心脏灌流方法,全心停灌30min和复灌120min模拟缺血/复灌损伤,测定心肌梗死面积、冠脉流出液中LDH含量。Westernblot测定缺血区心肌组织内皮一氧化氮合酶(eNOS)、磷酸化的内皮一氧化氮合酶(p-eNOS)蛋白的表达水平。结果:与缺血/复灌(I/R)组相比,HSYA治疗组心梗面积显著减少,并且乳酸脱氢酶(LDH)水平显著下降。NOS抑制剂L-NAME(10umol/L)可部分抵消HSYA对梗塞面积和LDH释放的保护作用。与对照组相比,HSYA组eNOS的磷酸化水平显著增高,而L-NAME可抑制其作用。结论:HSYA具有抗心肌缺血/复灌损伤的保护作用;HSYA抗心肌缺血/复灌损伤的作用机制可能与通过活化eNOS,增加NO生成有关。

The study of effect and mechanism of HSYA on ischemia/reperfusion injury

Objective:To determine whether HSYA protects the heart at reperfusion and whether nitric oxide (NO) acts in it. Method:Hearts isolated from male Sprague-Dawley rats were perfused on a Langendorff apparatus and subjected to 30 min global ischaemia, followed by 120 min reperfusion. Infarct size and the level of lactate dehydrogenase (LDH) in the coronary effluent were determined. Furthermore, levels of phosphorylated endothelial nitric oxide synthase (eNOS) protein were measured by western blot. Result:Pretreatment with HSYA for 5 min before ischaemia reduced infarct size and the release of LDH. 10 mmol/L NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS, attenuated the protective effects of HSYA.Levels of phosphorylated eNOS protein were significantly enhanced in the HSYA-treated group. Conclusion:The findings of the present study indicate that HSYA protects the myocardium against ischaemia–reperfusion injury through enhanced nitric oxide production by eNOS activation.