BDE-47慢性暴露对小鼠顶叶皮质、海马和丘脑的影响  

The Neurotoxic Effects of Chronic Exposure to 2,2’,4,4’-Tetrabromodiphenyl Ether on Mouse Parietal Cortex,Hippocampus and Thalamus Regions

作　　者：庄娟[1,2] 张佳琪[1,2] 汤潇 马心如 张丽娅 李梦秋 Zhuang Juan;Zhang Jiaqi;Tang Xiao;Ma Xinru;Zhang Liya;Li Mengqiu(Jiangsu Collaborative Innovation Center of Regional Modern Agriculture&Environmental Protection,Huaiyin Normal University,Huai’an 223300,China;Jiangsu Key Laboratory for Eco-Agricultural Biotechnology around Hongze Lake,School of Life Science,Huaiyin Normal University,Huai’an 223300,China;Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province,Jiangsu Normal University,Xuzhou 221116,China)

机构地区：[1]江苏省高校区域现代农业与环境保护协同创新中心,淮阴师范学院,淮安223300 [2]江苏省环洪泽湖生态农业生物技术重点实验室,淮阴师范学院生命科学学院,淮安223300 [3]江苏省药用植物生物技术重点实验室,江苏师范大学,徐州221116

出　　处：《生态毒理学报》2020年第5期228-234,共7页Asian Journal of Ecotoxicology

基　　金：江苏省高校自然科学基金资助项目(18KJB330001);江苏省环洪泽湖生态农业生物技术重点实验室开放基金资助项目(HZHLAB1707)。

摘　　要：为探讨2,2’,4,4’-四溴联苯醚(BDE-47)慢性暴露对脑顶叶皮质、海马和丘脑组织的影响及机制,小鼠经口腔灌胃20 mg·kg-1剂量的BDE-47,每日一次,共处理8周。检测小鼠脑相应组织的病理学变化、NLRP3表达、炎症因子IL-1β和IL-6的基因表达、小胶质细胞活化及细胞凋亡情况。结果表明,BDE-47慢性暴露使小鼠顶叶皮质、海马和丘脑组织神经细胞出现排列紊乱,神经元胞体固缩以及形态不规则等细胞形态学改变;并使小鼠顶叶皮质、海马和丘脑组织的NLRP3和Iba1蛋白表达增强,炎症因子IL-1β和IL-6表达增强,TUNEL信号加强。结果提示,BDE-47慢性暴露可损伤小鼠顶叶皮质、海马和丘脑组织,其毒性机制可能与NLRP3炎症小体介导的炎症反应和细胞凋亡异常增强有关。This study was aimed to investigate the toxic effects of chronic 2,2’,4,4’-tetrabromodiphenyl ether(BDE-47)exposure on mouse parietal cortex,hippocampus and thalamus regions and further to explore the underlying mechanisms.Mice were received 20 mg·kg-1 BDE-47 by oral gavage daily for 8 weeks.At the end of treatment,histopathological changes,immunofluorescence signals of NLRP3,gene expression of IL-1βand IL-6,microglial morphological changes and cell apoptosis in mouse parietal cortex,hippocampus and thalamus were evaluated.Our results showed that neuronal cells in mouse parietal cortex,hippocampus and thalamus regions were irregularly arranged and exhibited shrunken and irregular shapes after chronic BDE-47 exposure.BDE-47 raised the protein expression of NLRP3 and Iba1 in these brain regions of mice.Consistently,the levels of inflammatory cytokine IL-1βand IL-6 and TUNEL staining were also enhanced.These findings suggested that chronic exposure to BDE-47 may damage mouse parietal cortex,hippocampus and thalamus,and the underlying mechanism is probably correlated with NLRP3 inflammasome-mediated neuroinflammatory and enhanced cell apoptosis.

关 键 词：BDE-47 小鼠 神经毒性 NLRP3 神经炎症 细胞凋亡 

分 类 号：X171.5[环境科学与工程—环境科学]