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作 者:张宜波[1] 颜学军[2] 于常州[1] 曾因明[1]
机构地区:[1]徐州医学院江苏省麻醉学重点实验室,江苏徐州221002 [2]徐州医学院附属淮安医院麻醉科,江苏淮安223002
出 处:《南京医科大学学报(自然科学版)》2010年第6期806-809,共4页Journal of Nanjing Medical University(Natural Sciences)
基 金:江苏省普通高校自然科学研究计划(02KJD320031);淮安市科技发展计划资助(HAS03021)
摘 要:目的:观察黄芩素甙对脑缺血后大鼠海马CA1区神经元GluR2蛋白及其mRNA表达的影响。方法:SD雄性大鼠25只,体重250~300g,随机分成5组(n=5):假手术组(Ⅰ组)、缺血再灌注2天组(Ⅱ组)、缺血再灌注4天组(Ⅲ组)、黄芩素甙2天组(Ⅳ组)和黄芩素甙4天组(Ⅴ组)。后两组在缺血前30min给予黄芩素甙45mg/kg腹腔注射,其余各组在相应时间点给予等容量生理盐水。采用四血管阻断法制作大鼠全脑缺血再灌注模型,脑缺血时间10min。再灌注后2和4天再次麻醉动物,断头处死并分离海马CA1区,采用Western blot和RT-PCR技术分别测定GluR2及其mRNA的表达情况,并计算各自条带的灰度值。结果:与Ⅰ组比较,Ⅱ组和Ⅲ组的GluR2及其mRNA表达下调(P<0.01);与Ⅱ组和Ⅲ组比较,Ⅳ组和Ⅴ组的GluR2及其mRNA表达上调(P<0.01)。结论:黄芩素甙可能通过抑制脑缺血后海马CA1区神经元GluR2蛋白及其mRNA的下调而发挥脑保护作用。Objective:To investigate the effects of breviscarpin on GluR2 protein and mRNA expression in hippocampal CA1 neurons of rats following transient forebrain ischemia. Methods :Twenty-five male SD rats weighed from 250-300 g were randomly divided into 5 groups (n=5 each) :group Ⅰ (sham operation),group Ⅱ (ischemia/reperfusion for 2 days) , group Ⅲ (isehemia/reperfusion for 4 days) ,group Ⅳ(breviscarpin combined with ischemia/reperfusion for 2 days) ,group Ⅴ (breviscaipin combined with ischemia/reperfusion for 4 days). The rats of Ⅱ,Ⅲ,Ⅳ and Ⅴ group were subjected to transient but severe forebrain isehemia by permanently occluding the vertebral arteries and 24 hours later temporarily occluding the common carotid arteries for 10 minutes. Group Ⅰ animals were treated identically,except that the carotid arteries were not occluded. The rats of Group Ⅳ and Ⅴ were injected with breviscarpin (45 mg/kg) in abdominal cavity at 30 min before ischemia. The other groups were injected with equal 0.9% NaCl saline at the corresponding time. For quantization of GluR2 protein /GluR2 mRNA expression, rats were anesthetized and decapitated and the hippocampal CA1 were removed 2 days and 4 days after cerebral isehemia. GluR2 protein expression was assessed by Western Blot. RT-PCR was performed to assess the expression of GluR2 mRNA. The density of the bands was analyzed. Signal intensities were normalized against the internal standard (Western blot by GAPDH, RT-PCR by β-aetin). Results:The GluR2 protein and mRNA expressions of group Ⅱ and Ⅲ were both lower than those of group Ⅰ (P 〈 0.01 ). But the expressions of group Ⅳ and Ⅴwere higher than those of group Ⅱ and Ⅲ at the corresponding time (P 〈 0.01 ). Condusion:Breviscarpin attenuates down-regulation of GluR2 protein and mRNA after forebrain ischemia, which may be one of the inportant reasons rescuing hippocampal CA1 neurons after forebrain ischemia by breviscarpin.
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