热休克蛋白与神经保护  

Hsp70 and neuroprotection

作　　者：马波[1] 张建军[1] 刘耕陶[1] 

机构地区：[1]中国医学科学院·北京协和医学院药物研究所,中草药物质基础与资源利用教育部重点实验室,北京100050

出　　处：《中国药理学通报》2008年第8期984-987,共4页Chinese Pharmacological Bulletin

基　　金：国家重点基础研究发展规划(973规划)资助项目(No2007CB507400)

摘　　要：对脑中风患者,治疗时给予神经保护剂能挽救半暗带(penumbra),改善患者预后。缺血区ATP匮乏是脑损伤的始动因素,而神经元内蛋白质翻译停滞是脑缺血引起迟发性神经元死亡的标志。研究认为Hsp70高表达处于神经保护通路的上游关口,可以对抗缺血区的两大变化:蛋白质翻译停滞和ATP供给匮乏,抑制细胞凋亡和坏死,其机制与Hsp70参与蛋白折叠,抑制异常蛋白聚集,减少细胞毒性相关。因此,研究诱导Hsp70蛋白表达的药物对脑缺血的保护作用、阐明Hsp70诱导剂保护神经元的机制是很有意义的。Drag treatment with neuroprotective effect can rescue the penumbra induced by stroke and improve the living of patients. The ATP deficits in ischemic region initiate brain injury and translational inhibition of protein synthesis is a hallmark of delayed neuronal death after ischemia. HspTO overexpression is an early event in neuroprotective pathway and directly attenuates translational protein inhibition and ATP deficits induced by ischemia. The protective effects of Hsp70 result from its activity as a molecular chaperone assisting in correct protein folding and inhibit protein aggregation. Therefore, the development of Hsp70 inducer is significant for stroke patients and the protective mechanism remains to be investigated further.

关 键 词：HSP70 脑缺血 神经保护 蛋白翻译 

分 类 号：R329.25[医药卫生—人体解剖和组织胚胎学] R341[医药卫生—基础医学]