吗啡对脑缺血再灌注损伤后神经元凋亡及Bcl-2的影响

目的:探讨吗啡预处理对大鼠脑缺血再灌注损伤后神经元凋亡及Bcl-2蛋白表达的影响.方法:Wistar大鼠随机分为假手术组、模型组、吗啡组,各18只.四动脉阻断法建立脑缺血模型,吗啡组在脑缺血前60 min腹腔内注射吗啡1mg/kg.脑缺血8 min再灌注12h、72h及168h各取6只大鼠的脑组织,观察海马区病理学改变、神经元凋亡及Bcl-2表达.结果:吗啡预处理能使各灌注点海马神经元病理改变减轻、凋亡细胞数减少(P<0.01)、Bel-2表达增加(P<0.01).吗啡组细胞凋亡数减少趋势与Bcl-2表达上调趋势一致.结论:吗啡预处理可减轻缺血性脑损伤;吗啡抗凋亡作用机制与Bcl-2密切相关.

Effect of morphine on neuron apoptosis and Bcl-2 following cerebral ischemia-reperfusion injury

Objective:To investigate the effects of morphine preconditioning on neuron apoptosis and Bcl-2 protein expression in rats following cerebral ischemia-reperfusion injury. Methods:Wistar rats were randomly assigned to sham-surgery, model, and morphine groups, with 18 rats in each group. Global cerebral ischemia model were established using the four-vessel occlusion method. Rats from morphine group were intraperitoneally injected with 1 mg/kg morphine at 60 minutes before ischemia. After 8 minute cerebral iscbaemia Rat brains were removed at the end of predetermined duration of reperfusion 12h, 72h and 168h respectively to detect pathological changes,neuron apoptosis and Bcl-2 expression. Results:Morphine preconditioning significantly reduced the number of hippocampal apoptotic cells and increased number of Bcl-2 expression,and attenuated the neuronal pathological changes at each time point. The trend of neuronal apoptosis reduction was consistent with that of Bcl-2 increase. Conclusion:Morphine preconditioning could relicve ischemic brain injury Morphine anti-apoptotic mechanisms was closely related to Bcl-2.