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作 者:田悦[1] 郭善斌[2] 郭瑶[1] 黄威[1] 赵平[1]
机构地区:[1]中国医科大学附属盛京医院麻醉科,辽宁沈阳110004 [2]中国医科大学附属盛京医院药学部,辽宁沈阳110004
出 处:《中国现代医学杂志》2014年第23期15-18,共4页China Journal of Modern Medicine
摘 要:目的评价七氟醚后处理对β淀粉样蛋白1-40(Aβ1-40)诱导的大鼠认知功能障碍及海马内Aβ1-42含量的影响。方法 96只雄性SD大鼠,体质量250~300 g,采用随机数字表法将其分为4组,每组24只:生理盐水组(NS组)海马区注射生理盐水;淀粉样蛋白组(A组)海马区注射Aβ1-40;七氟醚后处理1组(S1组)和七氟醚后处理2组(S2组)海马区注射Aβ1-40,并于注射后28 d分别行2.5%七氟醚后处理2和4 h。各组于注射后28、35和42 d行水迷宫实验,并采用ELISA法测定各时点海马内Aβ1-42的含量。结果与NS组比较,A组、S1组和S2组各时点逃避潜伏期、上台前路程、无效搜索策略比例增加,海马内Aβ1-42含量升高(P〈0.05);与A组比较,S1组和S2组注射后42 d时逃避潜伏期、上台前路程和无效搜索策略比例增加,海马内Aβ1-42含量升高(P〈0.05);S1组和S2组各时点行为学指标及海马内Aβ1-42含量比较差异无统计学意义(P〉0.05)。结论七氟醚后处理可加重Aβ1-40诱导的大鼠认知功能障碍,其机制可能与七氟醚促进脑内Aβ1-42生成有关。[Objective ] To investigate the effect of Sevoflurane post-conditioning on cognitive dysfunction and expression of hippocampal endogenous Aβ1-42 in rats induced by Aβ1-40 [Methods] Ninty-six healthy male SD rats weighing 250-300 g were randomly divided into 4 groups (n =24): Normal saline group (group NS), Amyloid group (group A), Sevoflurane post-conditioning 1 group (group S1) and Sevoflurane post-condi- tioning 2 group (group S2). The animal model of Alzheimer's disease was established after Aβ1-40 was injected into bilateral hippocampus in rats of group A, group S1 and group S2, and the same volume of normal saline was injected in group NS. The animals of group S1 and S2 were anesthetized with 2.5% Sevoflurane which was maintained respectively for 2 h and 4 h on 28th day after injection-operation. Eight rats in each group performed Morris water maze test on 28th, 35th and 42th day after injection-operation and then were sacri- ficed to determine the content of Aβ1-42 in the hippocampus by ELISA. [Results] Compared with group NS, the escape latent period, swimming distance were significantly longer with more ineffective search tactics, and the content of Aβ1-42 was significantly increased at each time point in groups A, S1 and S2 (P〈0.05). Compared with group A, the escape latent period, swimming distance were significantly longer with more ineffec- tive search tactics, and the content of Aβ1-42 was significantly increased on 42th day after injection-operation in groups S1 and S2 (P〈0.05). There were no significant differences with regard to all above-mentioned indi- cators between groups S1 and S2 at each time point. [Conclusion] Sevoflurane post-conditioning can aggra- vate the cognitive dysfunction in rats induced by Aβ1-40 and the mechanism is probably related to increasing endogenous Aβ1-42 in hippocampus.
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