二氯乙酸对大鼠前脑缺血模型的保护作用。

Protective effect of dichloroacetate in a rat model of forebrain ischemia.

作者信息

Peeling J, Sutherland G, Brown R A, Curry S

机构信息

Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Canada.

出版信息

Neurosci Lett. 1996 Apr 12;208(1):21-4. doi: 10.1016/0304-3940(96)12542-8.

DOI:10.1016/0304-3940(96)12542-8

PMID:8731165

Abstract

Dichloroacetate (DCA) activates the pyruvate dehydrogenase complex (PDHC), and improves the recovery of cerebral pH, lactate, ATP, and PCr following reperfusion in animal models of forebrain ischemia. In order to determine whether this results in neuroprotection, rats were administered NaDCA (100 mg/kg or 10mg/kg i.v.) 10 min before 12 min of normothermic forebrain ischemia (bilateral carotid artery occlusion plus systemic hypotension, 45 mmHg). Neuronal injury assessed histopathologically 7 days post-ischemia was significantly reduced in the CA1 region of the hippocampus, the dorsal lateral striatum, and the neocortex, in rats treated with 100 mg/kg NaDCA, but not in rats treated with 10 mg/kg NaDCA.

摘要

二氯乙酸（DCA）可激活丙酮酸脱氢酶复合体（PDHC），并改善前脑缺血动物模型再灌注后脑pH值、乳酸、三磷酸腺苷（ATP）和磷酸肌酸（PCr）的恢复情况。为了确定这是否会带来神经保护作用，在常温下进行12分钟前脑缺血（双侧颈动脉闭塞加全身低血压，45毫米汞柱）前10分钟，给大鼠静脉注射二氯乙酸钠（NaDCA，100毫克/千克或10毫克/千克）。在缺血7天后通过组织病理学评估神经元损伤情况，结果显示，接受100毫克/千克NaDCA治疗的大鼠，其海马体CA1区、背外侧纹状体和新皮质的神经元损伤明显减轻，但接受10毫克/千克NaDCA治疗的大鼠则未出现这种情况。