褪黑激素对受损伤脑神经元的保护作用与bcl—2蛋白过度表达有关

研究：研究褪黑色激素对受损伤脑神经元的保护作用和对脑缺血后ｂｃｌ－２，ｂａｘ表达的影响。方法 用大鼠大脑中动脉梗死再灌注脑缺血模型，以脑梗死面积和存活细胞百分率作为脑损伤指标，用免疫组化的方法分析ｂｃｌ－２，ｂａｘ的表达。结果：缺血再灌注后２４ｈ褪黑激素呈剂量依赖性的减少脑梗死面积，减少缺血周边区细胞死亡，并显著增加该区ｂｃｌ－２的表达，而对ｂａｘ的表达则无明显影响。结论 褪黑激素具有明显减少缺血

Protective effect of melatonin on injuried cerebral neurons is associated with bcl-2 protein over-expression.

AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.