丹参多酚预处理对大鼠心肌缺血再灌注损伤的心肌保护

Protection of salvianolate proconditioning on myocardial ischemia in rats

目的:探讨丹参多酚预处理对大鼠心肌缺血再灌注损伤的保护作用及其可能的机制。方法:成年雄性SD大鼠缺血前1h给予丹参多酚(20mg/kg),结扎冠脉前降支缺血30min后,恢复灌注3h;应用2,3,5-氯化三苯基四氮(TTC)法检测心肌梗死面积;试剂盒检测乳酸脱氢酶(LDH)、肌酸激酶(CK)和髓过氧化物酶(MPO);心肌细胞的凋亡采用原位脱氧糖核苷酸末端转移酶介导的缺口末端标记(TUNEL)法检测;Western blot检测高迁移率族蛋B1(HMGB1)表达。结果:与对照组相比,丹参多酚预处理显著减小了心肌梗死面积,降低了心肌细胞凋亡和LDH、CK等血清心肌坏死标记物的表达(P<0.05)。丹参多酚预处理也显著降低了MPO的表达(P<0.05)。同时,丹参多酚预处理抑制了缺血再灌注引起的HMGB1的表达(P<0.05)。结论:丹参多酚预处理可以减轻心肌缺血再灌注损伤并抑制心肌细胞凋亡,其抑制缺血再灌注诱导的HMGB1的表达可能与这种保护作用相关。

Objective：To investigate the protection role of salvianolate and the mechanism by which salvianolate protects rats against myocardial ischemia and reperfusion （I/R） injury in rats. Method： Anesthetized male rats were treated with salvianolate （20 mg/kg） 1 h before ischemia,and then subjected to ischemia for 30 rain followed by reperfusion for 3 h. The lactate dehydrogenase（LDH）,creatine kinase （CK） and （MPO） were measured. Infarct size was measured by TTC and the myocardial tissue apoptosis was assessed by TUNNEL assay. HMGB1 ex- pression was assessed by Western blot. Result： Comparing with the control group, salvianolate could significantly decrease the infarct size,myocardium apoptosis and the levels of LDH and CK（P〈0.05）. Salvianolate could also significantly inhibit the increase in the MPO level（P〈0.05）. Meanwhile, salvianolate could also significantly inhibit the HMGB1 expression during myocardial I/R. Conclusion： Salvianolate precondtioning could reduce myocardial ischemia and reperfusion injury and myocardial tissue apoptosis by inhibiting HMGB1 expression.