癌变·畸变·突变2017，Vol.29Issue(3)：172-178,7.DOI:10.3969/j.issn.1004-616x.2017.03.003
2,2',4,4'-四溴联苯醚通过核受体介导神经毒性作用机制的初步研究
Preliminary study on mechanisms of neurotoxicity by 2, 2', 4, 4'- tetrabromodiphenyl ether via nuclear receptors
摘要
Abstract
OBJECTIVE: To investigate the effects of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) on cell proliferation and expression of the main nuclear receptors of RXRα,TRs and PPARs in human neuroblastoma SK-N-SH cells. METHODS:SK-N-SH cells were treated with different concentrations of BDE-47 and their proliferation was measured by the Cell Counting Kit-8 (CCK-8) assay. In addition,ROS level,SOD vitality,GSH-Px vitality and hOGG1 mRNA expression were analyzed by using the DCFH-DA,WST-1,colorimetric and qPCR assays,respectively. Involvement of the main nuclear receptors on expression of mRNA and protein were determined by qPCR and Western blot,respectively. RESULTS:BDE-47 inhibited cell proliferation and induced significant cytotoxicity in SK-N-SH cells. Dose- and time-dependent responses of the inhibitory effect were concentration-dependent,and the IC for 24-50 hours was 75.94 μmol/L. The expression levels in mRNA and protein of RXRα,TRs and PPARs in the treated cells were significantly increased compared with that in the control group,while induction of the isoforms was not consistent. CONCLUSION:BDE-47 inhibited proliferation of SK-N-SH cells via the induction of oxidative damage and neurotoxicity through up-regulating the expression of nuclear receptors:RXRα,TRs,and PPARs.关键词
2,2',4,4'-四溴联苯醚/视黄醛X受体/甲状腺激素受体/过氧化物酶体增殖物激活受体/氧化应激Key words
2,2',4,4'-tetrabromo diphenyl ether/retinoid X receptor/thyroid hormone receptors/peroxisome proliferator-activated receptors/oxidative stress分类
医药卫生引用本文复制引用
李云秀,蒋友胜,张建清,王晓辉,梅树江,周健,林晓仕,赵文钧,万克艳..2,2',4,4'-四溴联苯醚通过核受体介导神经毒性作用机制的初步研究[J].癌变·畸变·突变,2017,29(3):172-178,7.基金项目
国家自然科学基金(21677103,81260421) （21677103,81260421）
广东省科技厅产业技术研究与开发资金(2013B030800001) （2013B030800001）
