神经节苷脂联合依达拉奉对局灶性脑缺血再灌注大鼠PDK1、GSK3β蛋白表达的影响

Effects of monosialoganglioside and edaravone on expressions of PDK1,GSK3β protein in ischemic penumbra after focal cerebral ischemia/reperfusion in MCAO rats

目的观察单唾液酸神经节苷脂(GM1)联合依达拉奉对局灶性脑缺血再灌注大鼠缺血半暗带区PDK1、GSK3β蛋白表达的影响,探讨其可能的作用。方法随机将大鼠分为假手术组、模型组、GM1组(剂量20 mg/kg,腹腔注射,1次/d)、依达拉奉组(剂量3 mg/kg,腹腔注射,2次/d)、GM1联合依达拉奉组,采用线栓法制作大鼠大脑中动脉缺血再灌注模型,分别对缺血2 h后再灌注3、7、14 d,采用免疫组化Envision两步法检测大鼠模型缺血半暗带PDK1、GSK3β蛋白表达的阳性细胞平均吸收光密度和阳性面积单位。结果在缺血半暗带,再灌注3、7、14 d各时间点,GM1联合依达拉奉组PDK1蛋白表达平均吸收光密度和阳性面积单位分别显著高于GM1组、依达拉奉组(P<0.05)、模型组(P<0.01),GSK3β蛋白表达平均吸收光密度和阳性面积单位分别显著低于GM1组、依达拉奉组(P<0.01)、模型组(P<0.01)。结论 GM1联合依达拉奉能增强缺血半暗带PDK1蛋白表达,抑制GSK3β蛋白表达。

Objective To investigate the effects of GM1 and Edaravone on expressions of PDK1 ,GSK315 protein in ischemic penumbra after local cerebral ischemia/reperfusion in intraluminal thread occlusion of the middle cerebral artery rats and its related mechanism. Methods The local cerebral ischemia/reperfusion model was established by intraluminal thread occlusion of the middle cerebral artery. The animals were randomly divided into pseudo surgery group,model group, GM1 group, Edaravone group and GM1 and Edaravone group. Using the techniques of immu- no-histochemieal sraining,the expressions of PDK1, GSK3[5 protein were observed at 3,7 and 14 days in ischemic penumbra. Results In ischemic penumbra, 3,7,14 days each time point, a value and positive unit of the PDK1 protein expression in GM1 and Edaravone groups were higher than those in GM1 or Edaravone groups（P 〈 0. 05 ）, model groups（P 〈0. 01 ） ; a value and positive unit of the GSK3β protein expression in GM1 and Edaravone groups were lower than those in GM1 or Edaravone groups （P 〈 0. 01 ）, model groups （P 〈 0. 01 ）. Conclusion GM1 and Edaravone resist neural cell apoptosis,regulate PI3K/Akt signal transduction pathway by enhancing PDK1 protein and restraining GSK3 β expression after local cerebral ischemia/reperfusion in artery rats.