异丙酚对全脑缺血再灌注损伤大鼠的脑保护作用及其机制研究

目的探讨静脉麻醉药异丙酚对全脑缺血再灌注损伤大鼠的脑保护作用及其机制。方法成年雄性Wistar大鼠 19只 ,随机分为缺血组 (n =7)、异丙酚组 (n =7)和假手术对照组 (n =5 ) ,采用Pulsinelli法制备大鼠全脑缺血再灌注模型。异丙酚组再灌注开始后立即静脉输注异丙酚 1.5ml/h ,持续 3 0min。于再灌注 2 4h取脑 ,流式细胞仪检测凋亡率、坏死率、bcl 2、Bax和 p5 3蛋白在大鼠海马神经元中的表达情况。结果异丙酚可以降低大鼠全脑缺血再灌注 2 4h海马神经元的凋亡率和坏死率 (P <0 .0 5 ) ,与缺血组比较 ,异丙酚组Bax、p5 3的蛋白表达均降低 (P <0 .0 5 ) ,而bcl 2的变化无显著性差异 (P >0 .0 5 )。 结论异丙酚能降低大鼠全脑缺血再灌注神经元的凋亡率和坏死率 ,其机制可能与降低促凋亡基因Bax和 p5 3蛋白的表达有关

Cerebral protection effect and mechanism of propofol on global cerebral ischemia and reperfusion damage in rats

ObjectiveTo determine the cerebral protection effect and mechanism of propofol on global cerebral ischemia and reperfusion damage in rats.Methods19 adult male Wistar rats were randomly divided into 3 groups, ischemia group (n=7), propofol group (n=7), and sham injury group (n=5). Global cerebral ischemia and reperfusion model were made by means of Pulsinelli's method. Rats in propofol group were anesthesia with propofol at the dosage of 1.5 ml/h for 30 min at the beginning of reperfusion. Apoptosis and necrosis rate were detected by cytometry. In the same time, bcl 2, Bax and p53 protein expression in hippocampus neurons were detected. ResultsThe apoptosis and necrosis rate in propofol group were significantly decreased as compared with ischemia group ( P<0.05). Bax and p53 protein expression in hippocampus neurons were also significantly decreased as compared with ischemia group ( P<0.05), however, no significant findings in bcl 2 protein expression ( P>0.05).ConclusionPropofol can decrease apoptosis and necrosis rate in cerebral ischemia reperfusion injured neuron, and the mechanism maybe related to decreasing the expression of Bax, p53 protein.