Bcl-2腺病毒/E1B 19kD相互作用蛋白3对弥漫性轴索损伤后少突胶质细胞凋亡的调控作用

doi:10.16098/j.issn.0529-1356.2021.04.003

解剖学报 ›› 2021, Vol. 52 ›› Issue (4): 512-519.doi: 10.16098/j.issn.0529-1356.2021.04.003

Bcl-2腺病毒/E1B 19kD相互作用蛋白3对弥漫性轴索损伤后少突胶质细胞凋亡的调控作用

王婷婷¹ 穆娇¹ 李美玉¹于泓¹ 蒋丛政¹ 张晓丽² 张国徽^1*

1.河北北方学院法医学系; 2.河北北方学院生命科学研究中心，河北张家口 075000

收稿日期:2019-12-24 修回日期:2020-04-02 出版日期:2021-08-06 发布日期:2021-08-06
通讯作者: 张国徽 E-mail:18931316008@163.com
基金资助:
河北省自然科学基金

Role of Bcl-2 adenovirus/E1B 19kD interacting protein 3 in oligodendrocyte apoptosis after diffuse axonal injury

WANG Ting-ting¹ MU Jiao¹ LI Mei-yu¹ YU Hong¹ JIANG Cong-zheng¹ ZHANG Xiao-li² ZHANG Guo-hui^1*

1.Department of Forensic Medicine; 2.Life Science Research Center, Hebei North University, Hebei Zhangjiakou 075000, China

Received:2019-12-24 Revised:2020-04-02 Online:2021-08-06 Published:2021-08-06
Contact: ZHANG Guo-hui E-mail:18931316008@163.com

摘要/Abstract

摘要：

目的探讨Bcl-2腺病毒/E1B 19kD相互作用蛋白3（BNIP3）对大鼠弥漫性轴索损伤（DAI）后少突胶质细胞凋亡的调控作用。方法 77只SD雄性成年大鼠随机分为假手术组（11只）、DAI组（33只）及干预组（33只）。参照Marmarou方法制做DAI模型，干预组大鼠在打击后立即给予脑室注射BNIP3抑制剂necrostatin-1（Nec-1，30 g/L，2 μl），检测Nec-1干预前后DAI大鼠BNIP3蛋白表达，少突胶质细胞凋亡以及髓鞘的组织病理学变化。结果与假手术组相比，大鼠DAI损伤后脑干组织BNIP3表达上调，且与细胞凋亡成正相关； Nec-1干预有效降低DAI大鼠少突胶质细胞BNIP3蛋白表达，显著减少DAI大鼠少突胶质细胞凋亡的数目，提高DAI大鼠脑干髓鞘劳克坚牢蓝（LFB）染色平均吸光度和髓鞘碱性蛋白（MBP）表达，改善DAI大鼠脑干髓鞘的超微结构。结论 BNIP3参与DAI诱导的少突胶质细胞凋亡，抑制BNIP3可保护DAI大鼠少突胶质细胞和髓鞘。

关键词: 弥漫性轴索损伤, Bcl-2腺病毒/E1B 19kD相互作用蛋白3, 少突胶质细胞, 髓鞘, 免疫组织化学, 免疫印迹法, 大鼠

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 (MBP) 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.

Key words: Diffuse axonal injury, Bcl-2 adenovirus/E1B 19kD interacting protein 3, Oligodendrocyte, Myelin, Immunohistochemistry, Western blotting, Rat

中图分类号:

651.1⁺5

王婷婷穆娇李美玉于泓蒋丛政张晓丽张国徽. Bcl-2腺病毒/E1B 19kD相互作用蛋白3对弥漫性轴索损伤后少突胶质细胞凋亡的调控作用[J]. 解剖学报, 2021, 52(4): 512-519.

WANG Ting-ting MU Jiao LI Mei-yu YU Hong JIANG Cong-zheng ZHANG Xiao-li ZHANG Guo-hui. Role of Bcl-2 adenovirus/E1B 19kD interacting protein 3 in oligodendrocyte apoptosis after diffuse axonal injury[J]. Acta Anatomica Sinica, 2021, 52(4): 512-519.

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Bcl-2腺病毒/E1B 19kD相互作用蛋白3对弥漫性轴索损伤后少突胶质细胞凋亡的调控作用

Role of Bcl-2 adenovirus/E1B 19kD interacting protein 3 in oligodendrocyte apoptosis after diffuse axonal injury

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