热休克蛋白在脊髓损伤中的研究进展  

Research Progresses of Heat Shock Proteins in Spinal Cord Injury

作　　者：贺学岗 张广智 马占军[1,2] 高一诚 郭旭东 康学文[1,2] HE Xue-gang;ZHANG Guang-zhi;MA Zhan-jun;GAO Yi-cheng;GUO Xu-dong;KANG Xue-wen(Department of Orthopaedics,Lanzhou University Second Hospital,Lanzhou 730030,Gansu,China;Lanzhou University,Lanzhou 730030,Gansu,China)

机构地区：[1]兰州大学第二医院骨科,中国甘肃兰州730030 [2]兰州大学,中国甘肃兰州730030

出　　处：《生命科学研究》2020年第4期339-344,共6页Life Science Research

基　　金：脊柱疾患疼痛机制研究及治疗甘肃省国际科技合作基地项目(甘科外[2017]2号-34);国家自然科学基金资助项目(81371230);兰州大学第二临床医学院萃英学子科研培育计划(CYXZ2020-02)。

摘　　要：脊髓损伤(spinal cord injury, SCI)可造成损伤平面以下神经功能障碍,严重影响患者的生活质量。热休克蛋白(heat shock proteins, HSPs)是机体受到应激后保护细胞或组织,使其免受进一步伤害的重要分子之一,在脊髓损伤后表达升高,并通过促进血管生成、抑制炎症反应、抑制神经元凋亡、抗氧化应激等作用减缓脊髓损伤的进一步加重。本文主要就脊髓损伤后热休克蛋白的产生及其作用机制的研究进展进行综述,为后续相关研究提供参考。Spinal cord injury(SCI) can cause neurological dysfunction below the injury level, which seriously affects the patient’s quality of life. Heat shock proteins(HSPs) are one kind of the important molecules that protect cells or tissues from further injury after stress in the body. The expression of HSPs is increased after spinal cord injury, and the proteins can slow down further aggravation of spinal cord injury by promoting angiogenesis and inhibiting inflammatory response, neuron apoptosis and oxidative stress. Herein, the production and function mechanisms of HSPs after spinal cord injury are reviewed to provide reference for the related research in the future.

关 键 词：脊髓损伤(SCI) 热休克蛋白(HSPs) 继发性脊髓损伤 作用机制 

分 类 号：Q71[生物学—分子生物学] R744.9[医药卫生—神经病学与精神病学]