[The mechanisms of hippocampal neurons exposed to PBDE-209 induce oxidative stress and apoptosis].

ABSTRACT

OBJECTIVE: To determine the potential mechanisms of PBDE-209 induce apoptosis of the hippocampal neurons. METHODS: 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. RESULTS: 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. CONCLUSION: The oxidative stress and endoplasmic reticulum stress may involve in the apoptosis of nerve cells caused by PBDE-209.