依达拉奉对大鼠缺血/再灌注心肌细胞凋亡的影响

目的：观察依达拉奉对心肌缺血／再灌注后心肌细胞凋亡的影响。方法：选择30只健康SD大鼠，采用结扎冠状动脉左前降支后再通的方法复制心肌缺血再灌注的动物模型，随机分为假手术组（n=10）、缺血／再灌注（I／R）组（n=10）和药物（依达拉秦）组（n=10）。检测各组3h后心肌组织的超氧化物歧化酶（SOD）和丙二醛（MDA）的含量。并用免疫组化法测定局部凋亡相关因子Bcl-2、Fas的表达，比较各组间差异。结果：与假手术组比较，I／R组中反映氧化损伤程度的MDA明显升高（P〈0．01），抗氧化酶SOD则明显减少（P〈0．01），Fas含量升高（P〈0、01），Bcl-2含量明显减少（P〈0、01）；药物组较I／R组MDA含量明显减少（P〈0．01），SOD活性显著增加（P〈0．01），Fas含量明显降低（P〈0，05），Bcl-2含量明显增加（P〈0．01）。结论：依达拉奉具有抗心肌缺血再灌注损伤作用，其机制可能是通过调节Bcl-2和Fas介导的细胞凋亡而实现

Effects of edaravone on myocyte apoptosis induced by myocardial ischemia/reperfusion in rats

Objective To observe the effects of edaravone on cardiac myocyte apoptosis induced by myocardial ischemia/reperfusion(I/R) in rats. Methods Thirty rats were randomly divided into sham-operated group(n=10), I/R group(n=10) and edaravone treatment group(n=10). The animals subjected to 45 min myocardial ischemia followed by reperfusion for 3 h were sacrificed and their hearts were harvested. The activity of SOD and MDA, expression of Fas and Bcl-2 proteins in myocardial tissues in each group were measured. Results Compared with sham-operated group, the values of SOD and Bcl-2 were decreased significantly(P < 0.01, respectively) and the levels of MDA and Fas increased significantly(P < 0.01, respectively) in I/R group. However, the values of SOD,and Bcl-2 was lower (P < 0.05, P < 0.01, respectively) and the levels of MDA and Fas was higher(P < 0.05, repectively) in edaravone treatment group than those in I/R group. Conclusion Edaravone may protect myocardium from I/R injury by modulating the expression of Fas and Bcl-2 proteins and inhibiting apoptosis following myocardial I/R.