Clough-Helfman C, Phillis J W
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201.
Brain Res Bull. 1990 Jul;25(1):203-6. doi: 10.1016/0361-9230(90)90277-7.
Cerebral ischemic damage in gerbils was assessed by locomotor activity studies and histopathological examination of the hippocampal CA1 pyramidal cell layer. Pretreatment with AICAr (50 and 500 mg/kg) 30 min prior to a 5-min ischemic episode in unanesthetized gerbils, significantly attenuated the degree of ischemic neuronal damage as measured by either technique with the 500 mg/kg dose; the 50 mg/kg dose, although showing a trend, was not significant. A potential mechanism for AICAr-induced cerebroprotection may be that it is metabolized to uric acid, a free radical scavenger.
通过运动活动研究和海马CA1锥体细胞层的组织病理学检查，评估沙土鼠的脑缺血损伤。在未麻醉的沙土鼠缺血5分钟前30分钟，用AICAr（50和500mg/kg）预处理，500mg/kg剂量通过两种技术测量均显著减轻了缺血性神经元损伤的程度；50mg/kg剂量虽呈趋势但不显著。AICAr诱导脑保护的潜在机制可能是它被代谢为尿酸，一种自由基清除剂。
