PBDE-209 exposure damages learning and memory ability in rats potentially through increased autophagy and apoptosis in the hippocampus neuron
PBDE-209 exposure damages learning and memory ability in rats potentially through increased autophagy and apoptosis in the hippocampus neuron
复制标题
PBDE-209 暴露可能通过增加海马神经元的自噬和凋亡来损害大鼠的学习和记忆能力
DOI：
10.1016/j.etap.2017.02.006
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发表时间：
2017
影响因子：
4.3
通讯作者：
Chen Dunjin
中科院分区：
文献类型：
--
作者：
Sun Wen;Du Lili;Tang Wenting;Kuang Liyun;Du Peili;Chen Jingsi;Chen Dunjin
本研究旨在探讨妊娠期间PBDE-209通过胎儿海马神经元自噬和凋亡产生的神经毒性。海马组织和神经元中LC3-II和Beclin-1自噬蛋白水平显着升高，而P62蛋白水平较低。 PBDE剂量组中凋亡蛋白Cleaved Caspase-3和Cleaved PARP显着升高，高PBDE剂量组中BCL-2水平显着降低。在莫里斯水迷宫任务中，高PBDE剂量组的逃逸潜伏期明显更长。 PBDE-209 诱导的自噬导致神经元死亡，抑制自噬可减少 PBDE-209 诱导的细胞凋亡。这些结果表明，怀孕期间接触 PBDE-209 会增加海马自噬，降低神经元活力，并部分影响 PBDE-209 诱导的细胞凋亡。所有这些都可能导致后代学习和记忆能力下降。
This study is to investigate the neurotoxicity of PBDE-209 during pregnancy through autophagy and apoptosis in the fetal hippocampus neuron. The autophagy protein levels of LC3-II and Beclin-1 were significantly higher in hippocampus tissue and neuron, while P62 protein were lower. Apoptosis protein Cleaved Caspase-3 and Cleaved PARP was significantly higher in PBDE dose groups and BCL-2 levels in high PBDE dose groups were significantly lower. During the Morris water maze task, the escape latency times of high PBDE dose groups were significantly longer. PBDE-209-induced autophagy leads to neurons death and inhibition of autophagy reduce PBDE-209-induced apoptotic cell death. These results suggest that exposure of the PBDE-209 during pregnancy increases hippocampal autophagy, decrease neuron viability, and it partly effect apoptosis induced by PBDE-209. All that may contribute to the decline of learning and memory ability in the offspring.