本文關(guān)鍵詞： 腦缺血-再灌注 常壓高濃度氧 電壓依賴性陰離子通道蛋白 凋亡　出處：《首都醫(yī)科大學(xué)學(xué)報》2017年01期 　論文類型：期刊論文

【摘要】：目的 觀察常壓高濃度氧治療(normobaric hyperoxia,NBO)對腦缺血-再灌注大鼠電壓依賴性陰離子通道蛋白(voltage-dependent anion channel,VDAC)以及凋亡蛋白細胞色素C(cytochrome C,Cyt C)和活化型半胱天冬酶-3(cleaved caspase-3)的影響,初步探討其作用機制。方法 將15只健康成年雄性SD大鼠(280~320 g)采用數(shù)字表法分為3組:假手術(shù)組(Sham)、正常氧濃度組(Normoxia)和NBO組,采用線栓法制備大鼠大腦中動脈阻塞模型,模型大鼠缺血1.5 h,再灌注24 h。Sham組和Normoxia組大鼠術(shù)后呼吸普通空氣,NBO組大鼠術(shù)后至再灌注前呼吸100%常壓氧氣。采用Western blotting方法,檢測腦缺血半影區(qū)VDAC、Cyt C和cleaved caspase-3蛋白的表達變化。結(jié)果 1)與Sham組相比,Normoxia組缺血側(cè)半影區(qū)VDAC顯著升高(P0.05);與Normoxia組相比,NBO組缺血側(cè)半影區(qū)VDAC顯著降低(P0.05);2)與Normoxia組相比,NBO組缺血側(cè)半影區(qū)凋亡蛋白Cyt C和cleaved caspase-3顯著減少(P0.05)。結(jié)論 NBO治療可能通過調(diào)節(jié)缺血側(cè)半影區(qū)電壓依賴性陰離子通道蛋白VDAC的表達來抑制腦缺血誘發(fā)的細胞凋亡,從而實現(xiàn)腦神經(jīng)保護作用。
[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.
【作者單位】： 首都醫(yī)科大學(xué)宣武醫(yī)院北京市老年病醫(yī)療研究中心腦血管病研究室;
【分類號】：R743.3
【正文快照】： 線粒體是神經(jīng)細胞中極為重要的細胞器,不僅對物質(zhì)能量代謝和信號轉(zhuǎn)導(dǎo)等生理活動具有重要調(diào)節(jié)作用,而且在調(diào)控神經(jīng)細胞凋亡過程中起決定性作用。線粒體外膜電壓依賴性陰離子通道蛋白(voltage-dependent anion channel,VDAC)是線粒體依賴性凋亡過程中的關(guān)鍵蛋白,與細胞生存密切

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