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作 者:蒋向平 方开云[2] 何祥[2] 刚绍鹏[2] 文静[2] Jiang Xiangping;Fang Kaiyun;He Xiang;Gang Shaopeng;Wen Jing(School of Anesthesiology,Guizhou Medical University,Guiyang 550004,China;Department of Anesthesiology,People's Hospital of Guizhou Medical University,Guiyang 550002,China)
机构地区:[1]贵州医科大学麻醉学院,贵阳市550004 [2]贵州省人民医院麻醉科,贵阳市550002
出 处:《中华麻醉学杂志》2018年第11期1303-1306,共4页Chinese Journal of Anesthesiology
基 金:贵州省科技计划项目(黔科合基础[2016]1089号,黔科合SY字[2012]3107号,黔科合支撑[2019]2815号);贵州省科技合作计划(黔科合LH字[2015]1089号);贵州省人民医院博士基金(GZSYBS[2015]05号);贵阳市科技计划(筑科合[2013103]33号)。
摘 要:目的评价七氟醚诱发大鼠认知功能减退与大脑皮层α1A肾上腺素能受体(ADRA1A)的关系。方法清洁级健康成年SD大鼠48只,体重220~260g,3~4月龄,雌雄各半,采用随机数字表法分为2组(n=24):对照组(C组)和七氟醚组(S组)。S组吸入3%七氟醚5h。于麻醉后1和7d时行巴恩斯迷宫实验。于麻醉后即刻、麻醉后1和7d处死大鼠,取大脑皮层,采用Western blot法检测ADRA1A的表达,采用实时荧光定量PCR法检测ADRA1A mRNA的表达。结果与C组比较,S组各时点错误进洞数增多,进入目标洞的潜伏期和路程延长,大脑皮层ADRA1A及其mRNA表达下调(P<0.05)。结论七氟醚诱发大鼠认知功能减退的机制可能与大脑皮层ADRA1A表达下调有关。Objective To evaluate the relationship between sevoflurane-induced cognitive decline and α1A norepinephrine receptor(ADRA1A)in the cerebral cortex of rats.Methods Forty-eight clean-grade healthy adult Sprague-Dawley rats(24 male,24 female),weighing 220-260 g,aged 3-4 months old,were divided into 2 groups(n=24 each)using a random number table method:control group(group C)and sevoflurane group(S group).Group S inhaled 3% sevoflurane for 5 h.Rats underwent the Barnes maze test on days 1 and 7 after anesthesia.Rats were sacrificed immediately after anesthesia and on days 1 and 7 after anesthesia,and the cerebral cortex was removed for determination of the expression of ADRA1A protein and mRNA(by Western blot or fluorescent quantitative real-time polymerase chain reaction).Results Compared with group C,the number of entering incorrect holes was significantly increased,and the latency of entering the target hole and the distance were prolonged,and the expression of ADRA1A protein and mRNA in cerebral cortex was down-regulated at each time point in group S(P<0.05).Conclusion The mechanism of sevoflurane-induced cognitive decline is related to down-regulated expression of ADRA1A in the cerebral cortex of rats.
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