论文部分内容阅读
目的观察氟诱导小胶质细胞(MG)活化及其所致氧化损伤情况,探讨氟致中枢神经损伤的机制。方法培养小鼠小胶质细胞(BV-2),按0、0.5、1、2、10、50、100mg/L的氟化钠浓度染毒,采用细胞免疫化学方法测定小胶质细胞标记物OX-42的阳性表达情况,了解BV-2细胞活化状态:同时检测BV-2细胞或培养液中丙二醛(MDA)、谷胱甘肽(GSH)、超氧化物歧化酶(SOD)、一氧化氮合酶(NOS)、一氧化氮(NO)、过氧化氢(H2O2)和活性氧(ROS)含量。结果 5mg/L以上浓度氟化钠处理细胞24h后能够引起小胶质细胞的活化,OX-42表达的阳性细胞增加。50mg/L以上NaF染毒组细胞活力在氟处理24、48h后,显著降低,20mg/L以上NaF染毒组细胞活力在氟处理72h后显著降低,差异有统计学意义(P<0.05)。细胞染毒24h后,50、100mg/LNaF处理组细胞SOD活力显著低于对照组,差异有统计学意义(P<0.05);50mg/LNaF处理组细胞内的MDA含量显著高于对照组,差异有统计学意义(P<0.05);1、10、100mg/LNaF染毒组细胞内NOS和10、50、100mg/LNaF染毒组细胞培养液中NOS含量也显著高于对照组,差异有统计学意义(P<0.05)。结论一定剂量的氟可激活MG,释放活性氧自由基,可能在氟所致的中枢神经系统损伤中起一定的作用。
Objective To observe the activation of fluorine induced microglial cells (MG) and the oxidative damage induced by fluoride, and to explore the mechanism of fluoride-induced central nervous system injury. Methods Mouse microglial cells (BV-2) were cultured and treated with sodium fluoride concentrations of 0, 0.5, 1, 2, 10, 50 and 100 mg / L. Microglial cell markers OX-42 in BV-2 cells and the activation state of BV-2 cells were detected: the contents of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD) Nitric Oxide Synthase (NOS), Nitric Oxide (NO), Hydrogen Peroxide (H2O2) and Reactive Oxygen Species (ROS) Contents. Results Treatment with sodium fluoride at a concentration above 5 mg / L for 24 h resulted in activation of microglia and increased expression of OX-42. The cell viability of NaF exposed to 50mg / L or more of NaF was significantly decreased after 24 and 48h of F treatment. The viability of NaF exposed to 20mg / L or more of NaF was significantly lower than that of NaF exposed to 50mg / L for 72h (P <0.05). The cells in 50, 50mg / LNaF treatment group were significantly lower than the control group SOD activity after 24 hours of exposure (P <0.05); 50mg / LNaF treatment group cells MDA content was significantly higher than the control group, the difference (P <0.05). The concentrations of NOS in NOS and 10, 50 and 100 mg / L NaF groups were also significantly higher than those in control group Significance (P <0.05). Conclusion A certain dose of fluoride can activate MG and release reactive oxygen species, which may play a role in the damage of central nervous system induced by fluoride.