海马结构
细胞凋亡
氧化应激
切碎
膜联蛋白
海马体
丙二醛
内分泌学
内科学
化学
谷胱甘肽
免疫印迹
半胱氨酸蛋白酶3
程序性细胞死亡
男科
细胞生物学
生物
医学
生物化学
酶
基因
作者
Haofei Lin,Ruixue Dai,Jun Li,Yurong Li,Jing Tang,Jin Zhai
出处
期刊:PubMed
日期:2016-11-01
卷期号:45 (6): 977-983
摘要
To determine the potential mechanisms of PBDE-209 induce apoptosis of the hippocampal neurons.The primary fetal hippocampal neurons and hippocampus neurons cell line HT-22 were exposed to the concentrations of 0( solvent control), 6. 25, 12. 5, 25, 50 and 100 μg/mL PBDE-209 for 24 h. The SOD activity, MDA, NO and GSH contents in primary fetal hippocampal neurons were examined. The apoptosis of hippocampus neurons cell line HT-22 was observed using Annexin V/PI. The expressions of Bax, Bcl-2, CHOP, GRP78, PERK, Caspase-12 were measured by Western blot.The results showed that the difference was significant( P < 0. 05)of neuronal survival between the experimental groups and control groups and the difference was more obvious with the increasing dose of PBDE-209 which was observed in primary fetal hippocampal neurons and HT-22 cell lines. The increasing of Bax/Bcl-2( P < 0. 05), expression of CHOP and Caspase-12 in primary fetal hippocampal neurons( P < 0. 05), malondialdehyde( MDA) content and NO content( P < 0. 01) were also observed. Additionally, the results also indicated that PBDE-209 deceased activity of superoxidedismutase( SOD) and glutathione( GSH)( P < 0. 05). Meanwhile, the experiments of the HT-22 cell line showed that PBDE-209 could increase the expression of GRP78, PERK and Caspase-12 and apoptosis.The oxidative stress and endoplasmic reticulum stress may involve in the apoptosis of nerve cells caused by PBDE-209.
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