目的观察人参皂苷Rb1和Re对Aβ25-35诱导损伤SK-N-SH细胞的保护作用进而研究其内在机制。方法用Aβ25-35处理人神经母细胞瘤细胞(SK-N-SH细胞),模拟阿尔茨海默病的神经元损伤,并以适当浓度人参皂苷Rb1或Re处理。采用MTT法测定细胞存活率,荧光探针法检测细胞内ROS水平变化,Western blot法检测tau蛋白磷酸化水平及活性GSK-3β蛋白表达。结果培养基中添加Aβ25-35后SK-N-SH细胞存活率明显下降,而人参皂苷Rb1和Re均能显著提高损伤细胞的存活率,降低细胞内ROS水平,降低活性GSK-3β的表达,造成tau蛋白396位点的磷酸化程度下降,缓解tau蛋白的过度磷酸化。结论人参皂苷Rb1和Re对Aβ25-35诱导损伤的SK-N-SH细胞具有一定的保护作用。
Objective To investigate protective effects of ginsenoside Rb1 and Re against injury of SK-N-SH cells induced by Aβ25-35 and the possible mechanism.Methods Aβ25-35 was added to the medium for cell culture to make a cell model of Alzheimer disease,and ginsenoside Rb1 or Re were used to treat the injured cells.Cell survival rates were determined by the MTT assay,intracellular ROS levels were determined by fluorescence probes,and expressions of phosphorylated tau and active glycogen synthase kinase 3β(GSK-3β) were determined by Western blot.Results The survival ratio of SK-N-SH cells were significantly decreased after exposure to Aβ25-35,and treatment with ginsenoside Rb1 or Re significantly increased the survival ratio and decreased the cellular ROS level.Ginsenoside Rb1 and Re decreased expressions of phosphorylated tau and active GSK-3β,respectively.Conclusion Ginsenoside Rb1 and Re may exert a neuroprotective effect on SH-N-SH neural cells induced by neurotoxic Aβ25-35.