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目的:观察红景天苷对大鼠脑缺血-再灌注损伤后PI3-K、p-Akt及Caspase-3表达的影响。方法:将60只SD雄性大鼠随机分为假手术组12只、脑缺血-再灌注组(模型组)及红景天苷组(10 mg/kg)各24只。采用线栓法制备大鼠右侧大脑中动脉缺血-再灌注模型,观察缺血2 h再灌注6 h、12 h、24 h、48 h 4个不同时间点,采用Western Blotting法检测PI3-K、p-Akt及Caspase-3的蛋白表达。结果:与假手术组比较,模型组及红景天苷组4个不同时间点PI3-K、p-Akt、Caspase-3蛋白表达量均显著升高,差异均有统计学意义(P<0.01)。与模型组比较,红景天苷组4个不同时间点PI3-K、p-Akt蛋白表达量均升高,Caspase-3蛋白表达量均减少,差异均有统计学意义(P<0.05)。模型组及红景天苷组PI3-K、p-AKT蛋白表达趋势均从再灌注6 h开始逐渐升高,24 h达高峰,48 h较24 h下降,但高于12 h;Caspase-3蛋白表达趋势均从再灌注6 h开始逐渐升高,48 h达高峰。结论:红景天苷可能通过激活PI3-K/Akt信号转导通路,上调PI3-K、p-Akt的蛋白表达,抑制Caspase-3的蛋白表达,从而发挥对大鼠脑缺血-再灌注损伤抗凋亡的神经保护作用。
Objective: To observe the effect of salidroside on the expression of PI3-K, p-Akt and Caspase-3 after cerebral ischemia-reperfusion injury in rats. Methods: Sixty SD male rats were randomly divided into sham operation group (n = 12), cerebral ischemia - reperfusion group (model group) and salidroside group (10 mg / kg). The right middle cerebral artery occlusion (MCAO) model was established by thread occlusion method. The ischemia reperfusion injury was observed at 2 h, 6 h, 12 h, 24 h, 48 h after ischemia, and the PI3- K, p-Akt and Caspase-3 protein expression. Results: Compared with sham operation group, the expression of PI3-K, p-Akt and Caspase-3 in model group and salidroside group were significantly increased at 4 different time points, the difference was statistically significant (P <0.01 ). Compared with the model group, the expression of PI3-K and p-Akt protein increased and the expression of Caspase-3 protein decreased in all salidroside groups at 4 different time points (P <0.05). The expression of PI3-K and p-AKT in model group and salidroside group increased gradually from 6 h after reperfusion, reaching the peak at 24 h, decreasing at 24 h but higher than 12 h, while Caspase-3 The trend of protein expression increased gradually from 6 h after reperfusion, reaching the peak at 48 h. Conclusions: Salidroside can activate the PI3-K / Akt signaling pathway, up-regulate the protein expressions of PI3-K and p-Akt, and inhibit the protein expression of Caspase-3, Neuroprotective effect of anti-apoptotic injury.