丁苯酞对大鼠脑缺血再灌注损伤后凋亡相关因子表达的影响

Effects of dl-3n-butylphthalide on the expression of apoptosis-related factors in rats with focal cerebral ischemia-reperfusion

目的观察丁苯酞(NBP)对大鼠脑缺血再灌注损伤后脑组织Bcl-2和Bax表达的影响。方法 40只SD大鼠随机分为4组:假手术组、缺血再灌注组、溶剂对照组和丁苯酞治疗组,用线栓法,制作大鼠大脑中动脉脑缺血再灌注模型,于缺血2 h再灌注24 h后,断头取脑,用免疫组织化学法和RT-PCR法,观察脑组织Bcl-2和Bax表达水平的变化。结果大鼠脑缺血再灌注损伤后,Bcl-2和Bax显著增多;与模型组和对照组相比,治疗组Bcl-2的表达显著上调,Bax的表达显著下调,差异均有统计学意义(P<0.05)。结论丁苯酞对大鼠脑缺血再灌注损伤具有保护作用,其机制可能与上调Bcl-2的表达、下调Bax的表达有关。

Objective To observe the effects of dl-3n-butylphthalide（NBP） on the expression of Bcl-2 and Bax on cerebral ischemia-reperfusion injury in rats.Methods Forty male adult Sprague-Dawley rats were randomly assigned into four groups： sham operation group（sham group）,focal cerebral ischemia-reperfusion group（model group）,vehicle adminerstration group（vehicle group）,and dl-3n-butylphthalide group（NBP group）.The middle cerebral artery occlusion reperfusion model was made by the suture method（ischemia for 2 hours,and reperfusion for 24 hours）.After that,rats were sacrificed by decapitation,and the level of Bcl-2 and Bax expression were measured by immunohistochemical and RT-PCR.Results The expressions of Bcl-2 and Bax were increased significantly in rats with focal cerebral ischemia-reperfusion.Compared with model group and vehicle group,in rats of NBP group,the Bcl-2 expression was up regulated（P 0.05）,the Bax expression was down regulated（P 0.05）.Conclusion NBP can relieve the brain damage induced by focal cerebral ischemia-reperfusion in rats,which may significantly be related to the up regulation of Bcl-2 expression and the down regulation of Bax expression.