摘要
目的:观察不同浓度异丙嗪对大鼠急性前脑缺血再灌注线粒体通透性转换(MPT)的影响,并从分子水平探讨其神经保护作用的机制。方法:用夹闭双侧颈总动脉再开放法制作全脑缺血模型。大鼠随机分为缺血再灌注+异丙嗪组(治疗组),假手术+异丙嗪组(假手术组),缺血再灌注+NS(模型组);术前1 h静注不同浓度异丙嗪(5,15,45 mg/kg),术后6 h 3组均分离前脑线粒体,用分光光度法检测MPT值。结果:模型组分别与治疗组(异丙嗪浓度为5 mg/kg时)和假手术组(异丙嗪浓度为5,15 mg/kg时)比较,模型组MPT值减小更为明显(P<0.01);组内比较,异丙嗪浓度为5,15 mg/kg时比浓度为45 mg/kg时抑制MPT值减小的作用更为显著(P<0.05)。结论:异丙嗪能抑制缺血再灌注所致的MPT值的改变,因而可以通过阻止神经细胞线粒体的损伤发挥脑保护作用。
Objective： To observe the effects of promethazine at different concentrations on mitochondrial permeability transition（MPT）of acute ischemia-reperfusion in rat fore-brain, and to explore the neuron-protective mechanism in molecular level. Methods： Acute ischemia-reperfusion models in rat brain were made by reopening both sides common carotid artery after clipping. Rats were assigned into ischemia-reperfusion with promethazine group, sham operation with promethazine group and ischemia-reperfusion with normal saline group. Promethazine at different concentrations （5, 15, 45 mg/kg）were injected one hour before operation, the mitochondria were extracted from rat fore-head 6 hours after operation. The MFr value in all the groups was determined by spectrophotometer. Results： Compared with the groups of ischemia-reperfusion with promethazine（5 mg/kg）and sham operation with promethazine（5, 15 mg/kg）, the MPT value decreased significantly in the ischemia-reperfusion with normal saline group（ P 〈 0.01）. In the same group, the effect of promethazine（5, 15 mg/kg）was more obvious, compared with 45 mg/kg（ P 〈0.05）. Conclusion： Promethazine at various concentrations can inhibit the changes of MPT value induced by ischemia-reperfusion in rat fore-brain, therefore the neuron-protective effect may be produced by preventing neuron mitochondrial impairment.
出处
《汕头大学医学院学报》
2007年第1期33-35,共3页
Journal of Shantou University Medical College
关键词
异丙嗪
缺血再灌注
脑
线粒体膜的通透性转换
神经细胞保护
promethazine
ischemia-reperfusion, brain
mitochondrial permeability transition
protection of neuron
