步长脑心通对慢性脑缺血致血管性痴呆大鼠认知功能及神经细胞凋亡的影响

目的：通过观察步长脑心通对慢性脑缺血致血管性痴呆大鼠认知功能及神经细胞凋亡的影响，探讨步长脑心通治疗血管性痴呆的疗效和机制。方法：采用双侧颈总动脉永久结扎法制备前脑缺血大鼠模型，将造模成功的Wistar大鼠随机分为1月和2月模型对照组及给药组（步长脑心通），另设1月和2月正常对照组，每组6只大鼠。应用Morris水迷宫评定不同时期大鼠认知功能； 通过HE染色观察神经细胞的形态学改变；采用免疫组化方法对脑组织神经细胞凋亡率及Bcl-2蛋白表达水平进行检测。结果：Morris水迷宫检测结果表明，1月和2月给药组大鼠游迷宫平均潜伏期均明显低于模型对照组（P<0.01）；HE染色观 察发现，1月和2月给药组大鼠锥体细胞海马CA1区神经细胞缺血性改变较模型对照组改变轻，2月较1月给药组缺血改变明显；TUNEL染色观察发现，1月和2月给药组大鼠神经细胞凋亡率明显低于模型对照组(P<0.05)；给药组Bcl-2蛋白阳性细胞灰度平均值明显低于模型对照组(P<0.05)。结论：步长脑心通可明显提高Bcl-2的表达，抑制神经细胞凋亡，可用于治疗慢性脑缺血所致的认知功能障碍。

Effects of Buchang Naoxintong on cognitive function and apoptosis of cranial nerve cell in vascular dementia rats induced by chronic ischemia

Objective To explore the effects of Buchang Naoxintong on cognitive function and apoptosis of cranial nerve cells in vascular dementia rats induced by chronic ischemia and their mechanisms.Methods The permanent occlusion of bilateral common carotid arteries in Wistar rats was adopted to set up the chronic fore-brain ischemia model.Model rats were randomly divided into model control groups and drug groups at 1 and 2 month,unoperated Wistar rats were divided into normol control groups at 1 and 2 month,six rats in each group.The cognitive function was assessed by Morris water labyrinth.The morphologic changes of cranial nerve cells were observed with HE staining.The apoptosis was examined by methods of TUNEL,the expression of Bcl-2 protein was detected by immnunohistochemistry method.Results Compared with model control group,escape incubation periods in drug group at 1 and 2 month were shorter(P<0.01);the ischemia injury of the neurons of hippocampus CA1 was lighter,and the ischemia injury in drug group at 2 month was more serious than that at 1 month.The apoptotic rate of never cells in rats in drug group was lower than that in model group(P<0.05).The Bcl-2 protein expression in the rats treated with Buchang Naoxintong was lower than that in model group(P<0.05).Conclusion Buchang Naoxintong can increase the expression the Bcl-2 protein,restrain apoptosis of the cranial nerve cells and cure cognitive dysfunction induced by chronic ischemia.