依达拉奉对大鼠局灶性脑缺血再灌注后Caspase—3蛋白表达的影响

目的在大鼠脑缺血再灌注损伤发生后,用自由基清除剂依达拉奉对其进行治疗,监测再灌注不同时间点脑组织Cas-pase-3蛋白表达情况。研究依达拉奉对脑缺血再灌注损伤的保护作用。方法制作短暂、局灶性脑缺血再灌注模型。分为正常组及假手术组(对照组)、脑缺血再灌注对照组(缺血组)、依达拉奉治疗组(治疗组),分别于缺血1h后进行再灌注。治疗组于再灌注后30min腹腔内及皮下各注射依达拉奉1次(按依达拉奉3mg/kg),30min后重复一次。设再灌注后2h、6h、12h、24h、48h不同时间点,各时间点以0.4%戊巴比妥钠深度麻醉后快速断头法将大鼠处死,以4%多聚甲醛灌注固定后取脑,行免疫组化检测各时间点脑组织Caspase-3表达阳性细胞数。结果缺血组再灌注后2h在大脑额叶和顶叶皮质和海马即可见到Caspase-3蛋白表达的阳性细胞,12h达高峰,24h后开始下降。治疗组各时间点Caspase-3表达水平较对照组明显降低(P<0.01)。结论依达拉奉可抑制Caspase-3的表达,对缺血再灌注损害的脑组织有明显的保护作用。

Effects of edaravone on cerebral Caspase-3 protein expression after transient focal cerebral ischemia and reperfusion in rats

Objective Using the Edaravone to therapy the rats after transient focal cerebral ischemia and reperfusion To investigate whether neuroprotective effect can be achieved by Edaravone after transient focal cerebral ischemia;To testify whether the Caspase-3 protein expression in the pathogenesis of focal cerebral ischemia and reperfusion were involved by Edaravone.Methods Transient focal cerebral ischemia in rat models were set up The modles was divided into normal group,comtrol group,ischemia group:therap group.they were reperfusioned after 1 h of ischemia.The therapy group were ip and sc edaravone(3mg/kg) after 30 min of reperfusion,repeat it after 30 min.Made the rats death by the quick cutting head with 0.4% pintobabital sodium deep marcosis at 2 h?6 h?12 h?48 h after reperfusion.with the 4% paraformaldehyde to fix cerebral then take it out.Changing of cerebral Caspase-3 protein expression in the pathogenesis of focal cerebral ischemia and reperfusion were studied.Results The Caspase-3 protein expression cell can be seen in cerebral frontal and parietal cortex at the 2-hour point after reperfusion,which reached peak at the 12-hour point after reperfusion and decreased after the 24-hour point.The Caspase-3 protein expression cell in Edaravone-group was less significant than those in the control groups(P<0.01).Conclusion The Caspase-3 protein expression in cerebral cortex was restrained by Edaravone.The injury of focal cerebral ischemia and reperfusion were protected greatly by Edaravone.