摘要
目的:探讨促凋亡蛋白Bad的磷酸化p-Bad在局灶性脑缺血再灌注中的表达及依达拉奉的作用机制。方法:建立局灶性脑缺血再灌注大鼠模型;HE染色观察脑组织形态病理学变化;免疫组织化学法测定大鼠脑缺血再灌注不同时间磷酸化Bad的平均光密度值(A值)。结果:与假手术组比较,p-Bad在缺血再灌注2 h明显升高,于4 h达到峰值(P<0.05),随灌注时间延长表达逐渐减少并低于假手术组;依达拉奉干预组阳性表达在各时间点明显增加(P<0.05)。结论:脑缺血再灌注损伤可能导致Bad磷酸化活性增强,依达拉奉可通过上调p-Bad来发挥脑保护作用。
Objective：To explore the expresion of p-Bad in the model of foeial cerebeal ischemia-reperfusion and the effect of edaravone. Methods ：The model of focial cerebral ischemia-reperfusion injury was made. The pathological changes was observed by HE staining method. The average OD of the phosphorylation Bad was detected by immuno- histochemisery at different time after ischemia. Results ：Expression of p-Bad in model group was elevatory at 2 h after ischemia compared with the cham operation,it reached a peak level at 4 h after isehemia,then declined. Expression of p-Bad in edaravone treated group at all time points were significant increased. Conclusion：The protein expression of p- Bad may participated in the oecueance of ischemia cellular injury,edaravone obviously inhibited transient focal cerebral ischemia injury through up-regulate the expression of p-Bad and show a neuroprotective effect.
出处
《临床医药实践》
2010年第11期837-839,共3页
Proceeding of Clinical Medicine
