依达拉奉对大鼠脑缺血再灌注后 VEGF及Flk-1表达的影响

Effect of edaravone on regeneration of neurons in rats after cerebral ischemia/reperfusion injury

关键词:  缺血再灌注  VEGF  Flk-1  依达拉奉

Key words:  ischemia reperfusion  vascular endothelial growth factor  Flk-1  edaravone

摘要:

目的 探讨依达拉奉对大鼠脑缺血再灌注后VEGF及Flk-1表达的影响。方法 将脑缺血再灌注模型制备成功的雄性SD大鼠64只随机分成模型组、依达拉奉组,每组32只。试验后第2天,模型组予尾静脉注射生理盐水10ml/kg,依达拉奉组予依达拉奉3mg/kg,每日1次。在试验后第3、7、14、28天,两组各处死8只大鼠,大鼠处死前进行神经功能缺损评分。RT-PCR法检测纹状体VEGF及其受体Flk-1mRNA表达水平,ELISA检测纹状体VEGF蛋白水平。结果 实验后第7、14、28天,依达拉奉组神经功能缺失评分较模型组均显著降低,VEGF mRNA相对表达量、Flk-1mRNA相对表达量、VEGF蛋白相对表达量较模型组均显著升高(均P＜0.05)。依达拉奉组第7天神经功能缺失评分低于第3天,第14天低于第7天(均P＜0.05)。依达拉奉组第7天VEGF mRNA相对表达量、Flk-1mRNA相对表达量、VEGF蛋白相对表达量高于第3天(均P＜0.05)。结论 依达拉奉可改善脑缺血再灌注大鼠的运动神经功能,作用机制可能与促使纹状体VEGF及Flk-1表达,保护脑神经有关。

Abstract:

Objective To investigate the effect of edaravone on regeneration of neurons in rats after cerebral ischemia/reperfusion injury. Methods Sixty-four male SD rats with cerebral ischemia/reperfusion injury were divided into edaravone group(n=32) and model group(n=32). On the 2^nd day, rats in model group received intravenous injection of normal saline [10ml/(kg·d)] and rats in edaravone group received intravenous injection of edaravone [3mg/(kg·d)]. At the 3^rd, 7^th, 14^th, 28^th days, rats were sacrificed with 8 animals in each batch in both groups. Neural function defect scale was evaluated before sacrifice, and mRNA of VEGF and Flk-1 in corpus striatum was detected by RT-PCR, and VEGF protein was detected by ELISA. ResultsAt the 7^th, 14^th, 28^th day, neural function defect scale in edaravone group was significantly lower than that in model group. The expression of VEGF mRNA, Flk-1mRNA, and VEGF protein in corpus striatum of edaravone group was higher than that in model group. Neural function defect scale at d7 in edaravone group was lower than that at the 3^rd and 14^th days, the expression of VEGF mRNA, Flk-1mRNA and VEGF protein in edaravone group at the 7^th day was higher than that at the 3^rd day. Conclusion Edaravone can improve function of motor nerve in rats after cerebral ischemia/reperfusion injury, which may be associated with the up-regulation of VEGF and Flk-1 expression in corpus striatum.