人参皂苷Rb1对缺氧诱导N9细胞应激活化反应的影响

目的 探讨人参皂苷Rb1对缺氧诱导的小胶质细胞活化的的影响. 方法 通过人参皂苷Rb1对缺氧状态下N9细胞的干预,检测细胞形态、增殖活力改变.采用ELISA法、荧光探针DAF-FM DA、Griess Reagent法检测细胞TNF-α、O-2产量以及NO含量改变的影响.借助化学发光法、免疫荧光法分别检测各组细胞线粒体膜电位、细胞色素C含量. 结果 无论是预防性给药还是治疗性给药,人参皂苷Rb1能明显降低缺氧诱导活化的N9细胞NO、O-2以及TNF-α产量,抑制线粒体膜电位的降低,缓解细胞内细胞色素C含量的改变程度. 结论 人参皂苷Rb1均能在一定程度上下调由于缺氧活化导致神经毒性因子的高表达,稳定细胞线粒体的结构和功能,抑制缺氧诱导的N9细胞活化.

Effect of ginsenoside Rb1 on N9 cell activation induced by oxygen deficit

Objective To activate microglia N9 cell through the oxygen deficit, and to discuss the influence to the N9 cell by ginsenoside Rb1, laying the foundation for the basic study and the clinical medicine development. Methods Through ginsenoside Rb1 intervention, the cell morphology the proliferation ability were observed, ELISA, fluorescent probe DAF-FM DA, Griess the reagent examination, were used to measure TNF-α, the O-2 output, the NO content change, chemiluminescence, the immunofluorescence method, and plastochondria membrane potential, were carried out to detect the cytochrome C content. Results Regardless of being preventive or medical gives, ginsenoside Rb1 can decline the NO,O-2,TNF-α high expression; and reduce the plastochondria membrane potential changing, the cytochrome C redistribution. Conclusion Ginsenoside Rb1 can decline N9 cell activation to a certain extent, reduce expression of the nerve toxic factor, and to stabilize mitochondrial membrane potential and distribution of cytochrome C.