褪黑素对脑损伤神经元的保护作用与bcl-2蛋白过表达有关。

X Ling, L M Zhang, S D Lu, X J Li, F Y Sun
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引用次数: 0

摘要

目的:探讨褪黑素对脑缺血后神经元损伤的保护作用及其对bcl-2和bax表达改变的可能作用。方法:左大脑中动脉闭塞(MCAO)致大鼠脑缺血60 min。通过脑梗死面积和神经元计数评估脑损伤程度。免疫组化法分析bcl-2和bax的表达。结果:褪黑素可减少梗死面积,防止MCAO 1 h后24 h再灌注神经元死亡。缺血前给予褪黑素可增强半影区bcl-2的表达,对bax的表达无明显影响。结论:褪黑素能有效减轻缺血性脑损伤,增加缺血性脑神经元bcl-2的表达,提示褪黑素的保护作用与bcl-2在缺血神经元死亡中的上调有关。
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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.

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