BPI-1095对大鼠局灶性脑缺血后caspase-3蛋白表达的影响

目的观察BPI-1095对大鼠脑缺血后神经元caspase-3蛋白表达的影响。方法大鼠大脑中动脉闭塞缺血模型(n=90),随机分成6组:BPI-1095大剂量组(240mg/kg)、BPI-1095中剂量组(80mg/kg)、BPI-1095小剂量组(27mg/kg)、阿司匹林组(80mg/kg)、安慰剂组、假手术组。分析梗死面积百分数并观察各组Caspas-3蛋白表达。结果BPI-1095大、中剂量组梗死面积百分数小于安慰剂组(P<0.05);各组脑组织缺血周边和皮层caspase-3表达阳性细胞较安慰剂组减少,大剂量组caspase-3阳性细胞减少最多(P<0.05)。结论BPI-1095对大鼠永久性大脑中动脉闭塞模型的局灶脑缺血有神经保护作用,其作用机制与下调凋亡相关蛋白caspase-3的表达有关。

Effects of BPI-1095 on Caspase-3 in Middle Artery Occlusion Rats

Objective To investigate the effect of BPI-1095 on caspase-3 protein expression in middle artery occlusion(MCAO) rats.Methods Cerebral ischemia was induced with MCAO in adult male SD rats.Rats were randomly subjected into 6 groups with 15 rats in each group.Each rat has been given tested medication of different dosage and was sacrificed 24 h after treatment.The area of infarction was measured on each slice by image analysis system.Meanwhile,immunohistochemistry staining was used to identify caspase-3 expression in ischemic brain tissue.Results The infarcted area were significantly decreased in big and moderate dose treated rats(P<0.05,vs the placebo group).The expression of caspase-3 protein decreased in contralateral and ipsilateral hemisphere areas.The caspase-3 positive cell was significantly decreased in rats treated with big doses compared with placebo-or ASA-treated rats.Conclusion BPI-1095 shows neuroprotection in MCAO rats,which may related with the inhibition of caspase-3 expression resulting in apoptosis in penumbra.