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作 者:李昊[1] 宋春雨[1] LI Hao SONG Chun-yu(the Second Affiliated Hospital of Harbin Medical University,Harbin 150006 ,China)
机构地区:[1]哈尔滨医科大学附属第二医院,哈尔滨150006
出 处:《实用药物与临床》2017年第10期1107-1112,共6页Practical Pharmacy and Clinical Remedies
基 金:国家自然基金课题(304000393)
摘 要:目的研究丙泊酚是否能降低凋亡诱导因子(AIF)线粒体核转位,阻止Caspase非依赖性神经元凋亡,从而起到脑保护作用。方法 Wistar大鼠60只随机分为假手术组(S组)、缺血再灌注组(I/R组)、抑制剂组(I组)、丙泊酚组(P组)。S组大鼠仅接受手术而不遭受全脑缺血再灌注损伤打击;I/R组大鼠采用二血管夹闭法制造缺血模型10 min,然后再灌注;I组大鼠在缺血前2 min经静脉注入Caspase抑制剂;P组大鼠在全脑缺血再灌注前1 h,经股静脉持续泵注丙泊酚持续1 h,之后注入抑制剂,2 min后建立全脑缺血再灌注损伤模型。缺血再灌注后6、24、48 h,取海马组织用流式细胞仪测细胞凋亡率、Western blot法分析AIF线粒体核转位、凋亡相关基因Bax、Bcl-2的表达情况。结果与I/R、S、I组相比,P组神经元凋亡率显著降低,Bax/Bcl-2比值显著降低,AIF蛋白表达水平明显减少。结论丙泊酚对脑缺血再灌注损伤的脑保护作用可能与抑制海马神经元中AIF线粒体核转位有关。Objective To investigate whether propofol can reduce the apoptosis inducing factor( AIF),inhibit the nuclear translocation of mitochondria and prevent the apoptosis of Caspase independent neurons. Methods Totally60 Wistar rats w ere randomly divided into sham operation group( group S),ischemia reperfusion group( group I/R),inhibitor group( group I) and propofol group( group P). Rats in group S only underw ent surgery w ithout suffering from cerebral ischemia-reperfusion injury blow; rats in group I/R w ere established as blood deficiency model by tw o vessel clip preparation for 10 min,and then w ere given reperfusion; rats in group I w ere given intravenous injection of Caspase inhibitor at 2 min before ischemia; rats in group P w ere given intravenous continuous infusion of propofol via femoral vein for 1 h at 1 h before cerebral ischemia reperfusion,and then they w ere given intravenous injection of inhibitors,and the cerebral ischemia reperfusion injury model w as established after 2 min. The hippocampus w as taken,and the apoptosis rate w as measured by flow cytometry respectively at 6 h,24 h and 48 h after ischemia reperfusion; meanw hile,the expression of AIF nuclear translocation,Bax and Bcl-2 w ere analyzed by Western blot. Results Compared w ith group I/R,group S and group I,the apoptosis rate,ratio of Bax/Bcl-2 and the expression of AIF protein in group P decreased significantly( P〈0. 05). Conclusion The neuro-protective effect of propofol on cerebral ischemia reperfusion injury may be related to the inhibition of AIF nuclear translocation in hippocampus neurons.
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