三七总皂苷保护海马区神经元线粒体膜电位的实验研究

Protective effect of Panax notoginseng saponins on mitochondrial membrane potential of hippocampal neurons

目的研究三七总皂苷对缺血再灌注后海马区神经元线粒体膜电位的保护作用。方法36只SD大鼠随机分为假手术组、模型组、三七总皂苷组，每组12只。建立大鼠脑缺血再灌注模型，荧光染色流式细胞仪检测各组海马区神经元内游离Ca^2＋浓度和线粒体膜电位的变化。结果与假手术组比较，模型组海马区神经元内游离Ca^2＋浓度明显升高，线粒体膜电位明显降低（P〈0．01）；与模型纽比较，三七总皂苷组海马区神经元内游离Ca^2＋浓度明显降低（P〈0．01），线粒体膜电位明显升高（P〈0．05）。结论三七总皂苷能抑制缺血再灌注引起的海马区神经元内Ca^2＋浓度升高，抑制线粒体膜电位下降，保护海马区神经元线粒体功能，这可能是其抗脑缺血再灌注损伤的作用机制之一。

Objective To study the protective effect of Panax notoginseng saponins（PNS） on mitochondrial membrane potential（△ψm） of hippocampal neurons after cerebral ischemia-reperfusion. Methods Thirty-six rats were randomly divided into three groups,i, e. sham operation group,ischemia-reperfusion（model） group, PNS group. The model of cerebral ischemia-reperfusion was created by middle cerebral artery occlusion and recanalization. The concentration of free Ca^2＋ and △ψm of hippocampal neurons were assayed by flow cytometry. Results Compared with the sham operation group,the concentration of Ca^2＋ in hippocampal neurons of the model group increased significantly,and the △ψm decreased significantly （P 〈0.01）. Compared with the model group, the concentration of free Ca^2＋ in hippocampal neurons of the PNS group decreased significantly （P 〈 0.01）, and the △ψm increased significantly （P 〈0.05）. Conclusions PNS can inhibit the increase in concentration of free Ca^2＋ and the decrease in △ψm in hippocampal neurons induced by cerebral ischemia-reperfusion injury. It has protective effect on the mitochondrial function of the hippocampal neurons, which may be one of the mechanisms of the protective effects of PNS against injury induced by cerebral ischemia-reperfusion.