原花青素对脑缺血再灌注损伤大鼠Bcl-2表达和神经元凋亡的影响

目的探讨原花青素(PC)对脑缺血再灌注损伤大鼠Bcl-2表达和神经元凋亡的影响。方法将大鼠随机分为假手术组、缺血再灌注组、PC低剂量治疗组和PC高剂量治疗组,予相应药物灌胃1周,线栓法建立局灶性脑缺血再灌注模型。各组于缺血90 min再灌注24 h进行HE染色观察病理形态学变化,进行神经症状评分,采用TUNEL法检测神经细胞凋亡,免疫组化法观察大鼠额顶部皮质Bcl-2蛋白表达。结果①PC高、低剂量治疗组脑组织缺血损伤病理学改变明显轻于缺血再灌注组,PC高剂量治疗组缺血改变亦轻于低剂量治疗组。②PC高、低剂量治疗组神经功能缺损评分较缺血再灌注组降低(P<0.05)。③与假手术组比较,缺血再灌注组凋亡细胞明显增加,Bcl-2表达增加。与缺血再灌注组比较,PC高、低剂量治疗组均显著减少凋亡细胞,Bcl-2表达增加;高、低剂量组间比较亦具有显著性差异(P<0.05)。结论PC对缺血再灌注损伤脑组织具有保护作用,其机制可能是通过增加Bcl-2表达,抗神经元凋亡。

Influence of procyanidin on neural cell apoptosis and expression of Bcl-2 in rats with cerebral ischemic reperfusion injury

Objective It is to approach the influence of procyanidin on neural cell apoptosis and expression of Bcl-2 in rats with cerebral ischemia reperfusion(I/R) injury.Methods The rats were randomly divided into sham operated group,I/R group,low dose procyanidin treated group and high does procyanidin treated group,and were intragastric administration with corresponding physic liquor for 1 week.The focal middle cerebral artery occlusion(MCAO) model was made by thread-tie method. After 90 min MCAO following 24 h of reperfusion,HE staining and the neurological score was investigated.Neural cell apoptosis and expression of Bcl-2 was also investigated with TUNEL and immunohistochemistry.Results ①The change of ischemic impairment in the low or high dose procyanidin treated group was slighter than that of the IR group,and the change of the high dose procyanidin treated group was slighter than that of the low dose procyanidin treated group.②Compared with that of the IR group,the neurological score was decreased in the low and high dose procyanidin treated group(all P<0.05).③Compared with the sham operated group,the rate of neural cell apoptosis and expression of Bcl-2 were increased at 24 h of reperfusion in the ischemic territory(P<0.05).Compared with the I/R group,the expression of Bcl-2 was increased and the neural cell apoptosis rate was decreased in the low and high dose procyanidin treated group(P<0.05).There was significant difference between the low and high dose procyanidin treated group(P<0.05).Conclusion Procyanidin may reduce cerebral ischemia-reperfusion injure by increasing the expression of Bcl-2 and decreasing neural cell apoptosis.