Fas/FasL途径在氟暴露致PC12细胞凋亡中的作用

为了探讨Fas/FasL途径在氟暴露致PC12细胞凋亡中的作用及其机制，采用含20、40、80、160mg/L NaF培养液处理PC12细胞.结果表明，所有剂量NaF处理12、24、36、48h，PC12细胞活性升高；上述不同剂量NaF处理24h后，与对照组比，PC12细胞的活性氧水平、细胞凋亡率、细胞内Fas/FasL信号转导通路Fas和FasL、Caspase8、FADD、Caspase3基因和蛋白表达水平均呈显著上升（P < 0.05），而Bid基因和蛋白表达水平显著下降（P < 0.05），且呈氟暴露剂量依赖性.结果提示Fas/FasL途径在氟暴露致PC12细胞凋亡中起重要作用，其中FADD可能是Fas/FasL凋亡途径中的重要靶分子.

The role of Fas/FasL pathway in apoptosis of PC12 cells induced by fluoride exposure

The present study investigated the effects of exposure to fluoride on apoptosis of PC12 cells and aimed to clarify the role of Fas/FasL pathway involved in this effect. The results showed that treatment with NaF at 20, 40, 80, 160mg/L for 12, 24, 36, and 48hours enhanced the activity of PC12 cells, respectively. Treatment with all dosages of NaF for 24hours significantly increased the levels of reactive oxygen species (ROS) and apoptosis rate and dose-dependently up-regulated the gene/protein expression levels of Fas, FasL, Caspase8, FADD, and Caspase3, but down-regulated the gene/protein expression levels of Bid (P < 0.05). These results suggest that Fas/FasL apoptotic pathway plays an important role in the apoptosis of PC12 cells induced by fluoride exposure, in which FADD may be an important target molecule of fluoride exposure-induced apoptosis.