摘要
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Na F处理12、24、36、48h,PC12细胞活性升高;上述不同剂量Na F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Fas L、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 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.
作者
张佳勇
唐乐
于秋丽
阮琴
章子贵
ZHANG Jia-yong;TANG Le;YU Qiu-li;RUAN Qin;ZHANG Zi-gui(College of Chemistry and Life Science,Zhejiang Normal University,Jinhua 321004,China;College of Xing Zhi,Zhejiang Normal University,Jinhua 321004,China)
出处
《中国环境科学》
EI
CAS
CSCD
北大核心
2020年第6期2700-2707,共8页
China Environmental Science
基金
国家自然科学基金资助项目(81573101)。
