B cell lymphoma/leukemia-2 and adenovirus E1B19 000 interacting protein 3 in oligodendrocyte cell apoptosis following carbon monoxide poisoning

Abstract

Objective To investigate the role of B cell lymphoma/leukemia-2 and adenovirus E1B19 000 interacting protein 3(BNIP3) in oligodendrocyte cell apoptosis induced by carbon monoxide poisoning (CO poisoning) and the potential signal pathways. Methods Twenty-five male C57BL/6 mice were randomly divided into control group and CO poisoning group. Mice were left to breathe room air (control group) or subjected to 40-minute exposure to 2 500-3 000 ppm CO (CO poisoning group). The mice were sacrificed at 1, 3, 7 d and 14 d following CO poisoning. We examined the damage of myelin sheath and oligodendrocytes by observing the expression of myelin basic protein (MBP) and oligodendrocyte transcription factor 2 (Olig2) in corpus callosum. Furthermore, we explored the role of BNIP3 and potential signal pathways in the oligodendrocyte cell death following CO poisoning by observing the expression of BNIP3, Bcl-2 associated X protein (Bax) and cysteinyl aspartate specific proteinase 9 (caspase 9). Results Immunohistochemistry showed that the expression of MBP decreased significantly in the corpus callosum from 1 d (0.12±0.02, t=3.357, P 0.05), as compared with the control group(0.25±0.03). Moreover, compared with the control group(0.44±0.03), Bax was also upregulated in the corpus callosum from 1 d (1.09±0.15, t=9.427, P 0.05) compared with the control group (0.51±0.08). BNIP3 expression was positively correlated with Bax(r=0.995, P<0.01)and caspase 9 (r=0.950, P<0.01). Conclusion BNIP3 may play an important role in the apoptosis of oligodendrocytes induced by CO poisoning via the pathway of caspase dependent mitochondrial apoptosis. Key words: Apoptosis regulatory proteins; Carbon monoxide poisoning; Apoptosis; Mice