Valproic Acid: A New Candidate of Therapeutic Application for the Acute Central Nervous System Injuries

被引：57

作者：

Chen, Sheng ^{[1
]}

Wu, Haijian ^{[1
]}

Klebe, Damon ^{[2
,3
]}

Hong, Yuan ^{[1
]}

Zhang, Jianmin ^{[1
]}

机构：

[1] Zhejiang Univ, Sch Med, Dept Neurosurg, Affiliated Hosp 2, Hangzhou 310009, Zhejiang, Peoples R China

[2] Loma Linda Univ, Dept Physiol, Loma Linda, CA 92350 USA

[3] Loma Linda Univ, Dept Pharmacol, Loma Linda, CA 92350 USA

来源：

NEUROCHEMICAL RESEARCH | 2014年 / 39卷 / 09期

基金：

中国国家自然科学基金;

关键词：

Valproic acid; Brain injuries; Histone deacetylases inhibitor; Neuroprotection; HISTONE DEACETYLASE INHIBITORS; TRAUMATIC BRAIN-INJURY; SPINAL-CORD-INJURY; FOCAL CEREBRAL-ISCHEMIA; PROTECTS DOPAMINERGIC-NEURONS; PROMOTES FUNCTIONAL RECOVERY; MOOD STABILIZER; MEDIATED NEUROPROTECTION; BARRIER DISRUPTION; HEMORRHAGIC-SHOCK;

D O I：

10.1007/s11064-014-1241-2

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Acute central nervous system (CNS) injuries, including stroke, traumatic brain injury (TBI), and spinal cord injury (SCI), are common causes of human disabilities and deaths, but the pathophysiology of these diseases is not fully elucidated and, thus, effective pharmacotherapies are still lacking. Valproic acid (VPA), an inhibitor of histone deacetylation, is mainly used to treat epilepsy and bipolar disorder with few complications. Recently, the neuroprotective effects of VPA have been demonstrated in several models of acute CNS injuries, such as stroke, TBI, and SCI. VPA protects the brain from injury progression via anti-inflammatory, anti-apoptotic, and neurotrophic effects. In this review, we focus on the emerging neuroprotective properties of VPA and explore the underlying mechanisms. In particular, we discuss several potential related factors in VPA research and present the opportunity to administer VPA as a novel neuropective agent.

引用

页码：1621 / 1633

页数：13

共 106 条

[51] Neuroprotective effects of valproic acid against hemin toxicity: Possible involvement of the down-regulation of heme oxygenase-1 by regulating ubiquitin-proteasomal pathway [J].