Cho S, Joh T H, Baik H H, Dibinis C, Volpe B T
Laboratory of Molecular Biology, Cornell University Medical College at The Burke Medical Research Institute, White Plains, NY 10605, USA.
Brain Res. 1997 May 2;755(2):335-8. doi: 10.1016/s0006-8993(97)00188-1.
Melatonin administered at the beginning of cerebral reperfusion protected CA1 neurons against 10, 20 and 30 min of transient forebrain ischemia. Intraperitoneal injections of saline or melatonin (10 mg/kg) were given after 0, 2 and 6 h, or 1, 2 and 6 h of cerebral reperfusion, or 30 min prior to ischemia. One week later, quantitative histological analysis demonstrated that CA1 neuronal density was significantly increased in the melatonin groups that were treated at 0, 2, 6 h compared to the saline-treated controls. Ischemic protection of CA1 was lost in the animals in which the melatonin treatment was delayed by 1 h, or given 30 min prior to the ischemia.
在脑再灌注开始时给予褪黑素可保护CA1神经元免受10、20和30分钟短暂性前脑缺血的损伤。在脑再灌注0、2和6小时后,或1、2和6小时后,或缺血前30分钟腹腔注射生理盐水或褪黑素(10毫克/千克)。一周后,定量组织学分析表明,与生理盐水处理的对照组相比,在0、2、6小时接受褪黑素治疗的组中CA1神经元密度显著增加。在褪黑素治疗延迟1小时或在缺血前30分钟给予的动物中,CA1的缺血保护作用丧失。