常压高浓度氧下调电压依赖性阴离子通道蛋白对脑缺血-再灌注损伤大鼠的保护作用

发布时间：2018-01-30 15:40

本文关键词： 脑缺血-再灌注常压高浓度氧电压依赖性阴离子通道蛋白凋亡　出处：《首都医科大学学报》2017年01期 　论文类型：期刊论文

【摘要】：目的观察常压高浓度氧治疗(normobaric hyperoxia,NBO)对脑缺血-再灌注大鼠电压依赖性阴离子通道蛋白(voltage-dependent anion channel,VDAC)以及凋亡蛋白细胞色素C(cytochrome C,Cyt C)和活化型半胱天冬酶-3(cleaved caspase-3)的影响,初步探讨其作用机制。方法将15只健康成年雄性SD大鼠(280~320 g)采用数字表法分为3组:假手术组(Sham)、正常氧浓度组(Normoxia)和NBO组,采用线栓法制备大鼠大脑中动脉阻塞模型,模型大鼠缺血1.5 h,再灌注24 h。Sham组和Normoxia组大鼠术后呼吸普通空气,NBO组大鼠术后至再灌注前呼吸100%常压氧气。采用Western blotting方法,检测脑缺血半影区VDAC、Cyt C和cleaved caspase-3蛋白的表达变化。结果 1)与Sham组相比,Normoxia组缺血侧半影区VDAC显著升高(P0.05);与Normoxia组相比,NBO组缺血侧半影区VDAC显著降低(P0.05);2)与Normoxia组相比,NBO组缺血侧半影区凋亡蛋白Cyt C和cleaved caspase-3显著减少(P0.05)。结论 NBO治疗可能通过调节缺血侧半影区电压依赖性阴离子通道蛋白VDAC的表达来抑制脑缺血诱发的细胞凋亡,从而实现脑神经保护作用。
[Abstract]:Objective to observe the treatment of normobaric hyperoxia with high concentration oxygen under normal pressure. The effect of NBO on voltage-dependent anion channel in rats with cerebral ischemia-reperfusion was studied. VDAC), cytochrome cytochrome (Cyt C) and activated caspase-3 (caspase-3). Methods Fifteen healthy adult male SD rats were divided into 3 groups by digital table method: sham-operated group (Sham). Normal oxygen concentration group (Normoxia) and NBO group were used to establish the middle cerebral artery occlusion model of rats with ischemia for 1.5 h. The rats in the 24 h. Sham and Normoxia groups were breathing ordinary air after reperfusion. In NBO group, 100% normobaric oxygen was breathed from operation to reperfusion. Western blotting method was used to detect VDAC in cerebral ischemic penumbra. The expression of Cyt C and cleaved caspase-3 protein. Results 1) compared with Sham group. In Normoxia group, VDAC in ischemic penumbra increased significantly (P 0.05). Compared with Normoxia group, VDAC in ischemic penumbra decreased significantly (P 0.05). 2) compared with Normoxia group. The apoptotic protein Cyt C and cleaved caspase-3 in ischemic penumbra of NBO group decreased significantly (P 0.05). Conclusion NBO therapy may inhibit apoptosis induced by cerebral ischemia by regulating the expression of voltage-dependent anion channel protein VDAC in ischemic penumbra. Thus, the neuroprotective effect of the brain is realized.
【作者单位】：首都医科大学宣武医院北京市老年病医疗研究中心脑血管病研究室;
【分类号】：R743.3
【正文快照】： 线粒体是神经细胞中极为重要的细胞器,不仅对物质能量代谢和信号转导等生理活动具有重要调节作用,而且在调控神经细胞凋亡过程中起决定性作用。线粒体外膜电压依赖性阴离子通道蛋白(voltage-dependent anion channel,VDAC)是线粒体依赖性凋亡过程中的关键蛋白,与细胞生存密切

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