目的 探讨小檗碱对大鼠局灶性脑缺血再灌注损伤后神经功能评分及脑梗死体积,以及Bcl--2、Caspase-3表达的影响.方法 线栓法建立大鼠局灶性脑缺血再灌注损伤模型,大鼠随机分为模型组、小檗碱低、高剂量组(50,150 mg·kg-1·d-1)、假手术组(持续给药7 d,每日1次灌胃给药),脑缺血2 h再灌注24 h;分别在再灌注后3和24 h进行神经行为评分;并再灌注24 h后断头取脑.采用连续切片免疫组化技术检测脑组织中Bcl-2、Caspase-3表达的部位及数量.结果 小檗碱组神经功能评分明显低于手术对照组.脑梗死体积较模型组显著缩小.小檗碱组大鼠额顶部皮质Bcl-2、Caspase-3免疫阳性细胞数与模型组相比差异明显(P<0.05);同时小檗碱高剂量组大鼠额顶部皮质Bcl-2、Caspase-3免疫阳性细胞数与低剂量组比较差异显著(P<0.05).结论 小檗碱能明显减轻脑缺血再灌注损伤所造成的行为障碍,缩小梗死体积.可能通过上调皮质Bcl-2的表达、抑制Caspase-3的表达发挥脑保护作用.%Objective To determine the effects of berberine (BBR) on expression of Bcl-2, Caspase-3 after cerebral ischemia reperfusion (I/R) injury in rats and investigate the mechanism of anti-apoptosis effects of berberine on I/R cerebral injury. Methods Model of cerebral I/R injury was established by middle cerebral artery occlusion (MCAO). The rats were divided into model,sham and two BBR groups ( fed BBR with 150 or 50 mg· kg-1 · d -1 dose for 7 days). The score of neurological behavior was evaluated at the 3rd and 24th hours after reperfusion. The rats were put to death 24 h after reperfusion. The size of cerebral infarction was measured. Positive neurons of Bcl-2, Caspase-3 were observed by immunohistochemical method. Results Compared with model group, the injury degree of neuron and infarct volume were greatly reduced in BBR groups. Compared with sham operated group, the activities of Bcl-2, Caspase-3 were changed at 24 h reperfusion in the ischemic territory (P ＜0.05). Low and high dose BBR reduced the activities of Bcl-2 and Caspase-3 dose-dependently (P ＜ 0.05). Conclusions BBR can reduce the score of neurological behavior and infarct volume. BBR can raise Bcl-2 expression and reduce Caspase-3 expression in cerebral cortex and striatum of ischemia-reperfusion rat, which plays a role in brain protection.
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