Ling X, Zhang L M, Lu S D, Li X J, Sun F Y
Department of Neurobiology, Shanghai Medical University, China.
Zhongguo Yao Li Xue Bao. 1999 May;20(5):409-14.
To study the protective effect of melatonin against neuronal injury and the possible roles of alteration in the expression of bcl-2 and bax following brain ischemia.
Brain ischemia was induced by left middle cerebral artery occlusion (MCAO) for 60 min in rats. Brain damage was evaluated by the infarct area and the neuronal cell counting. The expression of bcl-2 and bax was analyzed by immunohistochemical method.
Melatonin decreased the infarct area and prevented the neuronal death after 24-h reperfusion following 1-h MCAO. Melatonin given before the ischemia enhanced the expression of bcl-2 in the penumbra area and had no significant effect on the expression of bax.
Melatonin effectively attenuated ischemic brain injury and increased the expression of neuronal bcl-2 in the ischemic brain, indicating that the protective effect of melatonin was associated with up-regulation of bcl-2 in ischemia-induced neuronal death.
研究褪黑素对神经元损伤的保护作用以及脑缺血后bcl-2和bax表达改变的可能作用。
通过大鼠左侧大脑中动脉闭塞（MCAO）60分钟诱导脑缺血。通过梗死面积和神经元细胞计数评估脑损伤。采用免疫组织化学方法分析bcl-2和bax的表达。
褪黑素减少了梗死面积，并在MCAO 1小时后24小时再灌注时防止了神经元死亡。缺血前给予褪黑素增强了半暗带区域bcl-2的表达，对bax的表达无显著影响。
褪黑素有效减轻了缺血性脑损伤，并增加了缺血脑中神经元bcl-2的表达，表明褪黑素的保护作用与缺血诱导的神经元死亡中bcl-2的上调有关。
