川芎素对脑缺血再灌注损伤细胞外信号调节激酶活化的影响

目的：观察大鼠局灶性脑缺血／再灌注后信号转导介质细胞外信号调节激酶(ERKs)的活化情况以及川芎素对其影响。方法：雄性成年SD大鼠45只，随机分成3组：假手术组、对照组和川芎素组(每组15只)，分别于缺血时腹腔注射生理盐水4ml，生理盐水4ml和川芎素100mg／kg(川芎素用4ml生理盐水溶解)。采用线栓法致大脑中动脉阻塞(MCAO)模型，在脑缺血再灌注后的2h、6h、12h、24h和72h分别处死大鼠(各组每个时间点3只)，将脑组织进行免疫组织化学和病理组织学染色观察。结果：病理组织学显示，缺血再灌注2h，川芎素组缺血侧皮层神经细胞缺血性损伤较对照组减轻。脑缺血诱导ERKs活化，第6h达高峰，并持续到72h。川芎素组ERKs活化明显较对照组增强，而且各时间点ERKs免疫反应阳性细胞数川芎素组显著较对照组增多(P<0．01)。结论：局灶性脑缺血再灌注可诱导缺血脑细胞部分ERKs活化，川芎素干预可使缺血大脑皮质ERKs活化增强，减轻皮层细胞的缺血性损伤。

Effect of Sodium Ferulate on Activation of Extracellular Signal Regulated Kinase after Cerebral Ischemia/Reperfusion Injury in Rats

Objective: To study the activation of extracellular signal regulated kinase (ERK) after focal cerebral ischemia/reperfusion in rats and the effect of sodium ferulate (SF) on it. Methods: Forty-five male adult SD rats were randomly divided into 3 groups, the sham-operated group, the control group and the SF group. The model of middle cerebral artery occlusion (MCAO) was established by thread ligation method, and in the ischemic phase, to rats in the sham-operated and the control group 4 ml of normal saline was intraperitoneally injected, and to rats in the SF group, 100 mg/kg of SF dissolved in 4 ml of normal saline was injected. The rats were decapitated at 2 hrs, 6 hrs, 12 hrs, 24 hrs and 72 hrs after reperfusion, 3 rats of every group at each time point, and rats brains were taken for immunohistochemistry and histopathological examination. Results: Histopathological examination showed that the cerebral ischemic damage in the SF group was significantly milder than that in the control group at 2 hrs after reperfusion. The cerebral ischemia induced ERK activation reached the peak at 6 hrs and maintained to 72 hrs after reperfusion. As compared with the control group, the ERK activation in the SF group was significantly enhanced with increased positive immune reacted cells (P<0.01). Conclusion: Cerebral ischemia/reperfusion could induce the activation of ERK in the ischemic brain cells, intervention of SF could enhance the activation and alleviate the ischemic injury in cerebral cortex.