Role of Bcl-2 adenovirus/E1B 19kD interacting protein 3 in oligodendrocyte apoptosis after diffuse axonal injury
10.16098/j.issn.0529-1356.2021.04.003
- Author:
Ting-Ting WANG
1
;
Jiao MU
1
;
Mei-Yu LI
1
;
Hong YU
1
;
Cong-Zheng JIANG
1
;
Guo-Hui ZHANG
1
;
Xiao-Li ZHANG
2
Author Information
1. Department of Forensic Medicine, Hebei North University
2. Life Science Research Center, Hebei North University
- Publication Type:Journal Article
- Keywords:
Bcl-2 adenovirus/E1B 19kD interacting protein 3;
Diffuse axonal injury;
Immunohistochemistry;
Myelin;
Oligodendrocyte;
Rat;
Western blotting
- From:
Acta Anatomica Sinica
2021;52(4):512-519
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of Bcl-2 adenovirus/E1B 19kD interacting protein 3 (BNIP3) in oligodendrocyte apoptosis after diffuse axonal injury (DAI) in rats. Methods Seventy-seven male adult Sprague-Dawley rats were randomly divided into sham group (n = 11), DAI group (n = 33), and intervention group (n = 33). DAI model was made referring to modified Marmarou method and the rats in intervention group received intracerebroventricular injection of BNIP3 inhibitor, necrostatin-1 (Nec-1, 30 g/L, 2 μl) immediately after injury. Tested the BNIP3 protein expression, oligodendrocyte apoptosis and myelin histopathology before and after the intervention of Nec-1. Results Compared with the sham group, DAI rats upregulated BNIP3 levels and had positive correlation with cell apoptosis in brainstem. Nec-1 significantly inhibited BNIP3 expression, then decreased the number of apoptotic oligodendrocytes, increased the average absorbance of luxol fast blue (LFB) staining and myelin basic protein (M BP) levels, and alleviated the myelin ultrastructure of DAI rats. Conclusion BNIP3 participate in the DAI-induced apoptosis of oligodendrocytes, and inhibition of BNIP3 can protect oligodendrocytes and myelin sheath from DAI injury.
