论文部分内容阅读
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、O2-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、O2-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。
Objective To investigate the effect of ginsenoside Rb1 on hypoxia-induced microglial activation. Methods Ginsenoside Rb1 on N9 cells in hypoxia intervention to detect cell morphology, proliferation and activity changes. The effects of changes of TNF-α, O2-production and NO content were detected by ELISA, DAF-FM DA and Griess Reagent. With chemiluminescence method, immunofluorescence method were used to detect mitochondrial membrane potential and cytochrome C content in each group. Results Ginsenoside Rb1 could significantly decrease the production of NO, O2- and TNF-α in hypoxia-inactivated N9 cells, inhibit the decrease of mitochondrial membrane potential, and alleviate the intracellular cytochrome C content, both in prophylactic and therapeutic groups The degree of change. Conclusion Ginsenoside Rb1 can down-regulate the high expression of neurotoxic factors due to hypoxia activation, stabilize the structure and function of mitochondria and inhibit the activation of N9 cells induced by hypoxia.