摘要
目的探讨依达拉奉对局灶性脑缺血损伤过程中脑细胞Caspase-3、Bcl-xl表达的影响及其机制。方法采用光镜、免疫组化方法检测大鼠局灶性脑缺血后梗死体积、病理变化及不同时间Caspase-3、Bcl-xl表达,应用依达拉奉对上述指标进行干预。结果局灶性脑缺血时Caspase-3、Bcl-xl的表达水平呈动态变化,Caspase-3表达于缺血24h达高峰,Bcl-xl表达于缺血6h达高峰,依达拉奉可使Caspase-3表达下降,Bcl-xl表达增加;依达拉奉能明显减小缺血后24h的梗死体积,减轻神经细胞损伤。结论依达拉奉干预可使脑缺血后Caspase-3表达减弱,Bcl-xl表达增强,缩小梗死体积,从而减轻神经元损伤。依达拉奉调整Caspase-3、Bcl-xl蛋白表达变化,可能是其脑保护作用机制之一。
Objective Investigate the effect of edaravone to Caspase-3 ,Bcl-xl during focal cerebral ische- mic in rats and its mechanism. Methods express in rats brain infarction volume ,pathological change and expres- sion of Caspase-3, Bcl-xl during different time were detected with light microscope, immunohistochemistry, these methods were applicated in rat which was injected edaravone. Results expression of Caspase-3 ,Bcl- -xl during fo- cal cerebral ischemic in rats are changeable, Caspase-3 reached a peak on 24h afle r ischemic, Bcl-xl reached the peak on 6h after ischemic, with edaravone , expression of Caspase-3 is decreased and Bcl-xl is increasing . edara- vone can decrease the volume of infarction after ischemic 24 hours obviously, lessen nerve injury. Conclusion edaravone can make expression of Caspase-3 decreased and Bcl-xl increased, deflate infarction volume, lessen nerve injury, edaravone modify the change of Caspase-3 and Bcl-xl,it is possibly one of cerebral protection mechanisms .
出处
《脑与神经疾病杂志》
2009年第2期111-113,共3页
Journal of Brain and Nervous Diseases
基金
吉林省科技厅自然科学基金资助项目(22050170
200705272)
