人参皂甙Rb1对大鼠脑缺血再灌注时神经元凋亡及Bcl-2和Bax表达的影响

目的观察人参皂甙Rb1(Ginsenoside Rb1,GRb1)对大鼠脑缺血再灌注时神经细胞凋亡及Bcl-2和Bax表达的影响,探讨GRbl的神经保护作用机制。方法阻塞大鼠大脑中动脉2 h制备脑缺血再灌注模型,大鼠随机分为缺血再灌注组(I/R组)和GRbl给药组(GRb1组),GRb1组大鼠在再灌注后立即腹腔注射GRb1(40 mg/kg)。两组再按不同的再灌注时间(3 h、12 h、1 d、2 d、3 d、5 d和10 d,每时间点4只)分为7个亚组。分别用HE染色、TUNEL染色和免疫组化染色观察神经组织病理改变、细胞凋亡、Bcl-2和Bax的表达。结果与I/R组相比,GRb1能减轻缺血侧脑组织的病理改变,减少神经细胞凋亡数(12 h、1 d、2 d和3 d时P<0.05),上调Bcl-2阳性细胞数(12 h、1 d、3d、5 d和10 d时P<0.05)和降低Bax阳性细胞数(3 h、12 h、1 d、2 d、3 d、5 d和10 d时P<0.05)。结论GRbl对脑缺血再灌注损伤有保护作用,其机制与抑制神经元凋亡、促进Bcl-2表达和抑制Bax表达有关。

Effects of Ginsenoside Rb1 on Neural Cell Apoptosis and Expressions of Bcl-2 and Bax in Rats Following Subjected to Cerebral Ischemia-reperfusion

Objective To observe the effects of Ginsenoside Rb1(GRb1) on neuronal cell apoptosis and the expressions of Bcl-2 and Bax in rats after cerebral ischemia-reperfusion so as to investigate the neuroprotective mechanism of GRb1.Methdos The model of cerebral ischemia-reperfusion was established by occluding rat middle cerebral artery for 2 h.The rats were randomly divided into two groups: ischemia-reperfusion group(I/R group) and GRb1 treat group(GRb1 group).GRb1(40 mg/kg,i.p.) was administered immediately to rats after the onset of reperfusion.Two groups were further subdivided 7 subgroups according to various reperfusion time(3 h,12 h,1 d,2 d,3 d,5 d and 10 d,n=4 per time point).HE staining was used to observe histological features.TUNEL and immunohistochemical method were used to analyze the cell apoptosis and expressions of Bcl-2 and Bax,respectively.Results Compared with I/R group,GRb1 reduced pathological changes,and decreased the number of apoptotic neural cells(P<0.05 on 12 h,1 d,2 d and 3 d) and up-regulated the number of Bcl-2 positive cells(P<0.05 on 12 h,1 d,3 d, 5 d and 10 d),and meanwhile down-regulated the number of Bax positive cells(P<0.05 on 3 h,12 h,1 d,2 d,3 d,5 d and 10 d) in the ipsilateral hemisphere.Conclusion The neuroprotective effect of GRb1 on cerebral ischemia-reperfusion injury is related to inhibit neuronal apoptosis and to up-regulate the expression of Bcl-2 with down-regulating the expression of Bax.