Yang Chao-Xian, Liu Jun-Xiang, Sun Zhu-Lei, Gao Xiao-Qing, Deng Li, Yuan Qiong-Lan
Department of Anatomy, Medical College, Tongji University, Shanghai 200029, China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2008 Mar;39(2):214-7.
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.
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.
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.
观察人参皂苷Rb1（GRb1）对脑缺血再灌注大鼠神经细胞凋亡及Bcl-2和Bax表达的影响，以探讨GRb1的神经保护机制。方法：采用大鼠大脑中动脉闭塞2小时建立脑缺血再灌注模型。将大鼠随机分为两组：缺血再灌注组（I/R组）和GRb1治疗组（GRb1组）。再灌注开始后立即给大鼠腹腔注射GRb1（40mg/kg）。根据不同再灌注时间（3小时、12小时、1天、2天、3天、5天和10天）将两组进一步细分为7个亚组，每个时间点n = 4。采用HE染色观察组织学特征。分别采用TUNEL法和免疫组化法分析细胞凋亡及Bcl-2和Bax的表达。
与I/R组相比，GRb1减轻了病理变化，减少了凋亡神经细胞数量（12小时、1天、2天和3天时P<0.05），上调了Bcl-2阳性细胞数量（12小时、1天、3天、5天和10天时P<0.05），同时下调了同侧半球Bax阳性细胞数量（3小时、12小时、1天、2天、3天、5天和10天时P<0.05）。
GRb1对脑缺血再灌注损伤的神经保护作用与抑制神经元凋亡、上调Bcl-2表达及下调Bax表达有关。
