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人参皂甙Rb1(GRb1)是人参中一个最重要的有效成分(人参属五加科中一属),能减少大鼠暂时性脑缺血梗塞面积和改善神经功能缺失症状,这种神经保护作用的机制不完全清楚。本实验研究GRb1的神经保护作用是否与防止神经元凋亡和调控神经元凋亡抑制蛋白(NAIP)的表达有关。通过阻塞大鼠大脑中动脉建立局灶性脑缺血模型,再灌注开始后立即给予腹腔注射GRb1(40mg/kg)。具有神经功能缺失的大鼠被随机分成2组:缺血组和GRb1组,每个组根据再灌注时间(3h,12h,1d,2d,3d,5d,10d,n=4/每时间点)分为亚组。正常大鼠和假手术组做为对照组。TUNEL标记分析凋亡细胞,用免疫组织化学的方法检测NAIP的表达。结果显示再灌注3h凋亡细胞数量开始升高,24h达高峰,后下降,但再灌注10d的凋亡细胞数量显著高于对照组(P<0.01)。与缺血组相比,GRb1各亚组的凋亡细胞数减少,但再灌注12h至3d,其差异具有统计学意义。在对照组,NAIP弱或阴性的免疫反应广泛出现在脑实质神经元。再灌注3h,NAIP阳性细胞增加,12h时达高峰,后下降。再灌注5d,NAIP阳性细胞数量比对照组少(P<0.05)。NAIP阳性神经元出现缺血性改变如扇形或三角形,纹状体星形胶质细胞强表达NAIP。在GRb1组,NAIP阳性细胞数量从再灌注12h到10d,显著高于缺血组。本实验结果提示大鼠局灶性脑缺血时,GRb1能减少细胞凋亡,其机制可能与增加NAIP的表达有关。
Ginsenoside Rb1 (GRb1) is one of the most important active ingredients in ginseng (a genus of Panax quinquefolium) and can reduce the transient cerebral ischemic infarct size and improve the symptoms of neurological deficits. This neuroprotective effect The mechanism is not completely clear. This study investigated whether the neuroprotective effect of GRb1 is related to the prevention of neuronal apoptosis and the regulation of neuronal apoptosis inhibitory protein (NAIP) expression. The model of focal cerebral ischemia was established by blocking the middle cerebral artery of rat, and GRb1 (40 mg/kg) was injected intraperitoneally immediately after the start of reperfusion. Rats with neurological deficits were randomly divided into 2 groups: ischemia group and GRb1 group, each group according to reperfusion time (3h, 12h, 1d, 2d, 3d, 5d, 10d, n=4/per time point) Divided into subgroups. Normal rats and sham groups served as control groups. Apoptotic cells were analyzed by TUNEL labeling and the expression of NAIP was detected by immunohistochemistry. The results showed that the number of apoptotic cells began to increase at 3h after reperfusion, peaked at 24h and then decreased, but the number of apoptotic cells at 10d after reperfusion was significantly higher than that of the control group (P<0.01). Compared with the ischemic group, the number of apoptotic cells decreased in each subgroup of GRb1, but the difference was statistically significant between 12h and 3d after reperfusion. In the control group, NAIP weak or negative immune responses occurred extensively in brain parenchymal neurons. After 3 hours of reperfusion, NAIP-positive cells increased, peaked at 12 hours, and then decreased. After 5 days of reperfusion, the number of NAIP-positive cells was less than that of the control group (P<0.05). NAIP-positive neurons show ischemic changes such as a fan or triangle, and striatal astrocytes strongly express NAIP. In the GRb1 group, the number of NAIP-positive cells was significantly higher than that of the ischemic group from 12h to 10d after reperfusion. The results of this experiment suggest that GRb1 can reduce apoptosis in rats with focal cerebral ischemia, and its mechanism may be related to increased expression of NAIP.