竹节参总皂苷对大鼠局灶性脑缺血/再灌注神经元凋亡的影响

Effects of Total Rhizome Panacis Japonica Saponins on Apoptosis in Rats Following Cerebral Ischemia and Reperfusion

目的:研究竹节参总皂苷(total rhizome panacis japonica saponins,tRPJS)对大鼠局灶性脑缺血再灌注后神经细胞凋亡的影响及机制。方法:采用大鼠右侧大脑中动脉阻断(middle cerebral artery occulusion,MCAO)局灶性脑缺血再灌注模型,大鼠随机分为假手术组、损伤模型组、tRPJS不同剂量组(50、100、200mg.kg-1ip),观察各组大鼠神经功能状态,应用TUNEL法和免疫组化染色分别检测神经凋亡细胞数及bcl-2、Bax蛋白表达。结果:与损伤模型组比较,tRPJS治疗组可明显改善大鼠神经功能的受损程度,并减少神经细胞凋亡数,明显增加bcl-2蛋白表达,减少Bax蛋白表达,并呈剂量依赖性。结论:tRPJS在局灶性脑缺血再灌时具有抗神经细胞凋亡作用,改善受损的神经功能,从而对脑缺血再灌注损伤起保护作用,其机制可能与上调bcl-2蛋白,下调Bax蛋白的表达有关。

Objectives：To study the effects of（total rhizome panacis japonica saponins,tRPJS）on apoptosis and the expression of bcl-2 and Bax following cerebral ischemia and reperfusion and evaluate the protecting mechanism of tRPJS.Methods：tRPJS at dose 50,100 or 200 mg·kg^-1was intraperitoneally injected once a day for 4 days.The focal cerebral ischemia-reperfusion model was established with thread embolism in middle artery before tRPJS injection on the fourth day.Neurological deficit function score of rats was evaluated;and immunohistochemical and TUNEL technique was carried out to detect the expression of bcl-2,Bax and changes of apoptotic cell.Results：Compared with the control group,the deficit score of neural function was significantly improved;The expression of bcl-2 positive cells was increased significantly and the expression of Bax positive cells in tRPJS treated group was decreased significantly.Conclusions：tRPJS can decrease apoptosis by up-regulating bcl-2 and down-regulating Bax,so tRPJS has the neuro-protective effect against ischemia reperfusion injury