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神经突蛋白对大鼠实验性创伤性脑损伤具有神经保护作用。

Neuritin provides neuroprotection against experimental traumatic brain injury in rats.

作者信息

Liu Qi, Zhang Hang, Xu Jian, Zhao Dong

机构信息

a Department of Neurosurgery , First Affiliated Hospital of Medical College, Shihezi University , Shihezi , Xinjiang , China.

b The Key Laboratory of Xinjiang Endemic and Ethnic Diseases , Medical College of Shihezi University , Shihezi , Xinjiang , China.

出版信息

Int J Neurosci. 2018 Sep;128(9):811-820. doi: 10.1080/00207454.2018.1424155. Epub 2018 Jan 24.

DOI:10.1080/00207454.2018.1424155
PMID:29334295
Abstract

OBJECTIVES

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Neuritin is a neurotrophic factor that regulates neural growth and development. However, the role of neuritin in alleviating TBI has not been investigated.

METHODS

In this study, Sprague Dawley rats (n = 144) weighing 300 ± 50 g were categorized into control, sham, TBI and TBI + neuritin groups. The neurological scores and the ultrastructure of cortical neurons, apoptotic cells and caspase-3 were measured by using Garcia scoring system, transmission electron microscopy, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, Western blot analysis and real-time RT-PCR at various time points post-TBI.

CONCLUSIONS

Our findings indicated that neuritin plays a protective role in TBI by improving neurological scores, repairing injured neurons and protecting the cortical neurons against apoptosis through inhibition of caspase-3 expression. Further investigation of the molecular mechanisms underlying caspase-3 inhibition by neuritin will provide a research avenue for potential TBI therapeutics.

摘要

目的

创伤性脑损伤(TBI)是全球范围内死亡和残疾的主要原因。神经生长素是一种调节神经生长和发育的神经营养因子。然而,神经生长素在减轻TBI方面的作用尚未得到研究。

方法

在本研究中,将体重300±50 g的144只Sprague Dawley大鼠分为对照组、假手术组、TBI组和TBI+神经生长素组。在TBI后的不同时间点,使用Garcia评分系统、透射电子显微镜、末端脱氧核苷酸转移酶介导的dUTP缺口末端标记、蛋白质印迹分析和实时RT-PCR测量神经功能评分、皮质神经元的超微结构、凋亡细胞和半胱天冬酶-3。

结论

我们的研究结果表明,神经生长素通过改善神经功能评分、修复受损神经元以及通过抑制半胱天冬酶-3表达保护皮质神经元免受凋亡,从而在TBI中发挥保护作用。进一步研究神经生长素抑制半胱天冬酶-3的分子机制将为潜在的TBI治疗提供研究途径。

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