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作 者:程青格[1] 徐平[1] 龚其海[2] 史艳红[1] 刘赛[1] 黄艺婧[1]
机构地区:[1]遵义医学院附属医院神经内科 [2]遵义医学院药理学教研室,贵州遵义563099
出 处:《遵义医学院学报》2012年第5期379-382,共4页Journal of Zunyi Medical University
基 金:贵州省科技厅社发攻关项目(NO:黔科合SY字[2010]3074)
摘 要:目的观察反式白藜芦醇(TR)对β淀粉样蛋白(Aβ25-35)致痴呆大鼠海马caspase12 mRNA和蛋白表达的影响,补充说明TR抗痴呆的作用机制。方法大鼠随机分为五组:假手术组、阳性对照组、模型组、低剂量组、高剂量组,每组9只。在大鼠海马给予Aβ25-35造模结束后连续灌胃15 d每日1次,阳性对照组给予多奈哌齐1mg/kg,低剂量给予TR10mg/kg,高剂量TR40mg/kg,假手术组和模型组给予同体积的生理盐水。第15天时处死大鼠,免疫组化及Western blot检测海马caspase12蛋白表达,实时定量PCR检测海马caspase12 mRNA的表达。结果大鼠注射Aβ25-35后,模型组海马caspase12蛋白和mRNA表达明显高于假手术组(P<0.01)。TR剂量依赖性地降低了大鼠caspase12蛋白表达和mRNA表达(P<0.05)。结论 TR抗Aβ25-35致痴呆大鼠的作用机制与抑制海马caspase12基因表达有关。Objective To observe the effects of tran -resveratrol (TR) on hippocampus caspasel2 mR- NA and protein expressions in Aβ25-35 -induced dementia rats and further explore the anti -dementia mechanisms of trans - resveratrol. Methods Rats were randomly divided into sham, positive control (donepezil), model (Aβ25-35) , low - and high - dose of TR groups, respectively (n =9). After the injection of Aβ25-35 into hippocampus, rats were administrated with 1.0 mg/kg donepezil and 10 and 40 mg/kg TR once daily by gavage for consecutive 15 days, while sham and model groups were administrated with volume - matched normal saline by gavage. After the final treatment, all the rats were sacrificed and caspasel2 protein expression was examined by immunohistochemistry and western blotting assay and easpase12 mRNA expression was detected by real time PCR in rat hippocampus. Results Compared with the sham group, Aβ25-35 increased the protein and mRNA expressions of caspase12 in rat hippocampus (P 〈 0.01 ). Compared with the model group, TR treatments significantly decreased the protein and mRNA expressions of caspase12 in rat hippocampus in dose - dependent manner (P 〈 0.05 ). Conclusion The mechanisms underlying TR-mediated anti-dementia induced by Aβ25-35 might be, at least partly, due to the decreased expression of caspase12 in rat hippocampus.
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