摘要
目的研究人参皂甙Rbl(Ginsenoside Rb1,GRb1)对大鼠脑缺血再灌注时神经细胞凋亡及神经细胞凋亡抑制蛋白(NAIP)、Bcl-2和Bax蛋白表达的影响,探讨人参皂甙Rbl的神经保护作用机制。方法阻塞Wistar大鼠大脑中动脉制备短暂性脑缺血模型,出现神经功能缺失症状的大鼠随机分为缺血组和GRb1组,GRb1组大鼠在再灌注后立即腹腔注射人参皂甙Rb1(40mg/kg)。每组按不同的再灌注时间(3h、12h、1d、2d、3d、5d和10d,每时间点4只)分为7个亚组。分别用原位未端标记法和免疫组织化学方法观察凋亡细胞、神经元凋亡抑制蛋白(NAIP)、Bcl-2和Bax的表达。结果与缺血组相比,GRb1组的各亚组凋亡细胞数下降,但只在再灌注12h^3d时有显著差异;GRb1组的NAIP阳性细胞数在再灌注12h^10d时明显高于缺血组;GRb1组的Bcl-2阳性细胞数在再灌注12h^10d时显著上升,Bax阳性细胞数则在相同时间点下降。结论人参皂甙Rbl通过促进NAIP、Bcl-2表达和抑制Bax表达发挥神经保护作用。
Objective To study the effects of Ginsenoside Rb1 （GRb1） on neuronal cell apeptosis and the expressions of neuronal apoptosis inhibitory protein （NAIP）, Bcl-2 and Bax in rats after cerebral ischemia-reperfusion in order to investigate the neuroprotective mechanism of GRb1. Methods Transient cerebral ischemia was induced by middle cerebral artery occlusion （MCAO） in Wistar rats. GRb1 （40mg/kg,i. p. ） was administered immediately after the onset of reper- fusion. The rats with neurological deficits were randomly divided into 2 groups： ischemic group and GRb1 group. Each group was further divided into subgroups according to various reperfusion time （ 3h, 12h, 1,2,3,5,10days, n = g per time point）. Apeptotic cells were analyzed using an in situ Apep Tag kit. Immunohistochemical method was used to assess expression of neuronal apeptosis inhibitory protein （NAIP） ,bcl-2, and bax. Results Compared with ischemia group,the apoptotic cells decreased at all subgroups of GRb1 ; however, the significant differences were only found from 12h to 3d of reperfusion. In the GRb1 group,the number of NAIP-pesitive cells from 12h to 10d after ischemia was evidently higher than in the ischemia group. The number of bcl-2-pesitive cells was significantly increased from 12h to 10d after reperfusion in comparison with the ischemia group;however, the number of bax-pesitive cells significantly declined at the same time points as compared to ischemia group. Conclusion Our findings suggest that GRb1 has neuroprotective effect due to increased expression of NAIP and bcl-2,and reduced expression of bax.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2008年第1期12-16,共5页
Journal of Apoplexy and Nervous Diseases
