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Abstract

Role of Neuronal Nrdp1-USP8-Hypoxia Inducible Factor-1 Alpha Signal Axis in Hypoxic Injury after Cerebral Ischemia

Author(s): Leifang Yang, Bin Ren* and Yangjun Han
Department of Neurosurgery, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi Province 030032, 1Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province 430030, 2Neurointervention Center, Shanxi Cardiovascular Hospital, Taiyuan, Shanxi Province 030000, China

Correspondence Address:
Bin Ren, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province 430030, China, E-mail: xucludvvd2325@163.com


To investigate the role of neuromodulin receptor degradation protein-1-ubiquitin-specific protease 8-hypoxia inducible factor alpha signal axis in neuronal hypoxic injury after cerebral ischemia. 20 clean-grade healthy male Sprague-Dawley rats and 2 pregnant rats about 17 d of gestation were randomly selected. The rat model of cerebral ischemia was established and the rats were divided into control group (n=10) and model group (n=10). The pregnant mice were killed, the primary cortical neurons were obtained and cultured, and the target gene was connected to the shuttle plasmid to construct adenovirus vector. Western blotting and real time quantitative fluorescence polymerase chain reaction were used to detect the expression of neuromodulin receptor degradation protein-1 in each group and the expression of neuromodulin receptor degradation protein-1 in cortical neurons induced by hypoxia at different time. Apoptosis of neurons in each group was detected by in situ terminal deoxynucleotidyl transferase dUTP nick end labeling. The expression levels of neuromodulin receptor degradation protein-1, apoptosis-related proteins poly (ADP-ribose) polymerase, Bcl 2-associated X protein, B-cell lymphoma 2, ubiquitin-specific protease 8 and hypoxia-inducible factor alpha were measured by Western blotting. Compared with the control group, the expression of neuromodulin receptor degradation protein-1 in the model group was raised. After hypoxia treatment, the expression of neuromodulin receptor degradation protein-1 in cerebral cortical neurons increased. Compared with neuromodulin receptor degradation protein-1 interference control group, the expression level of neuromodulin receptor degradation protein-1, proteins poly (ADP-ribose) polymerase and Bcl-2-associated X protein in neuromodulin receptor degradation protein-1 interference group were decreased, while the expression level of B-cell lymphoma 2, ubiquitin-specific protease 8 and hypoxia-inducible factor alpha were increased.

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