李振伟¹,
刘畅¹,
李春娜¹,
邵静¹,
李亚晨¹,
李双月¹,
刘晓晖^1,,,
韩璐^2,,
1. 大连医科大学公卫学院劳动卫生与环境卫生教研室, 大连 116044;
2. 大连医科大学附属妇产医院, 大连 116033

作者简介: 李振伟(1987-),女,硕士研究生,研究方向为劳动卫生与环境卫生,E-mail:448019522@qq.com.

通讯作者: 刘晓晖,liuxh892@126.com ; 韩璐,13940801858@163.com

基金项目: 国家自然科学基金(81273031,81302400)
辽宁省自然科学基金(2013023054)
大连医科大学引进人才基金(201069)
大连理工大学工业生态与环境工程教育部重点实验室开放基金(KLIEEE-12-04)


中图分类号: X171.5

Toxic Effect and Mechanism of BDE 47 on Neuro-2a Cells

Li Zhenwei¹,
Liu Chang¹,
Li Chunna¹,
Shao Jing¹,
Li Yachen¹,
Li Shuangyue¹,
Liu Xiaohui^1,,,
Han Lu^2,,
1. Department of Environmental Health and Toxicology, School of Public Health, Dalian Medical University, Dalian 116044, China;
2. The Maternity Affiliated Hospital of Dalian Medical University, Dalian 116033, China

Corresponding authors: Liu Xiaohui,liuxh892@126.com ; Han Lu,13940801858@163.com

CLC number: X171.5

-->

摘要
HTML全文
图(0)表(0)
参考文献(0)
相关文章
施引文献
资源附件(0)
访问统计

摘要:探讨2,2',4,4'-四溴联苯醚(2,2',4,4'-tetrabromodiphenylether,BDE 47)对神经细胞Neuro-2a的毒性影响及机制。将Neuro-2a细胞暴露于浓度为6.25、12.5、25、50、100 μmol·L^-1的BDE 47,采用MTT法检测细胞存活率、荧光探针DCFH-DA检测细胞活性氧生成量、吖啶橙检测溶酶体膜通透性、罗丹明123检测细胞线粒体膜电位、Annexin V-FITC检测细胞凋亡、Western blot检测组织蛋白酶B (Cathespin B)表达。结果显示,与对照组相比,12.5、25、50、100 μmol·L^-1 BDE 47显著降低Neuro-2a细胞存活率和细胞线粒体膜电位(P<0.05);6.25、12.5、25、50、100 μmol·L^-1 BDE 47显著诱导活性氧含量升高(P<0.05),增加Neuro-2a细胞溶酶体膜通透性(P<0.05),诱导Neuro-2a细胞凋亡(P<0.05),升高Cathespin B蛋白表达(P<0.05)。结果表明,BDE 47可能通过介导溶酶体-活性氧-线粒体环路,诱导Neuro-2a细胞凋亡。
关键词: BDE 47/
Neuro-2a/
神经毒性/
溶酶体/
线粒体/
活性氧/
凋亡

Abstract:In order to explore the neurotoxicity of BDE 47, Neuro-2a cells were exposed to 6.25, 12.5, 25, 50 and 100 μmol·L^-1 BDE 47 for 24 h. MTT was used to evaluate the cell viability, DCFH-DA was used to detect the production of reactive oxygen species (ROS), acridine orange (AO) was used to evaluate the lysosomal membrane permeability (LMP), rhodamine 123 was used to observe the mitochondrial membrane potential (MMP), Annexin VFITC was used to investigate the apoptosis, Western blot was used to detect the protein expression of cathepsin B. The results showed that compared with the control, 12.5, 25, 50, 100 μmol·L^-1 BDE 47 decreased the viability and MMP of Neuro-2a cells (P<0.05), respectively. And 6.25, 12.5, 25, 50, 100 μmol·L^-1 BDE 47 increased the production of ROS, LMP, apoptosis and the expression of cathepsin B (P<0.05), respectively. These results indicated that BDE 47 might induce apoptosis of Neuro-2a cells via lysosomal-ROS-mitochrondial cross-talk pathway.
Key words:BDE 47/
Neuro-2a/
neurotoxicity/
lysosomal/
mitochondrial/
ROS/
apoptosis.