NADPH氧化酶在氟诱导小胶质细胞氧化应激中的作用

目的：观察NADPH氧化酶在氟引起的小胶质细胞氧化应激中的作用,为进一步研究氟致中枢神经系统损伤机制提供实验依据.方法：用1,5,10,25,50,100 mg/L的氟化钠处理BV-2小胶质细胞6,12,24h后,检测细胞活力、细胞内活性氧（ROS）含量,以及NADPH氧化酶抑制剂API处理后的小胶质细胞ROS水平变化情况.结果：BV-2小胶质细胞细胞氟化钠染毒后,细胞活力显著降低,差异有统计学意义（P＜0.05）.染毒组细胞内ROS含量显著高于对照组,差异有统计学意义（P＜0.05）.与单独染氟组相比,NADPH氧化酶抑制剂API能够显著降低氟化钠诱导的BV-2细胞内活性氧（ROS）含量.结论：氟能引起小胶质细胞氧化应激,NADPH氧化酶在氟诱导的ROS产生中起一定作用。

The effects of NADPH oxidase on the oxidative stress induced by fluoride in BV-2 microglia cells

Objective： To observe the effect of NADPH oxidase on the oxidative stress of BV--2 ceils treated by fluoride and to understand the mechanism of fluoride--induced damage to central nervous system. Methods：BV--2 microglia eeUs were treated with 1, 5, 10, 25, 50 and 100mg/L NaF for 6,12,24h,and MTT and intraeeUular ROS were measured. Results ：BV--2 cells viability decreased remarkably at NaF--treated cells for 12 and 24 h, and there were significant negative correlations between cell viability and NaF concentrations. Compared with the control cells, ROS increased significantly in 50 and 100mg/L NaF--treated cells. Compared with the cells with only fluoride treatmen, pretreated of BV--2 cells with NADPH oxidase inhibitor API dramatically decreased NaF--indueed ROS generations （P〈0.01）. Conclusion：Fluoride could induce microglia to produce more ROS, which possibly resulted in central nervous system damage.