Effect of Sevoflurane post-conditioning on cognitive dysfunction and expression of hippocampal endogenous Aβ_(1-42) in rats induced by Aβ_(1-40)
Yu Tian
Abstract
Yu Tian
Abstract
【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-conditioning 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 28 th day after injection-operation. Eight rats in each group performed Morris water maze test on 28 th, 35 th and 42 th day after injection-operation and then were sacrificed 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 ineffective search tactics, and the content of Aβ1-42 was significantly increased on 42 th day after injection-operationin groups S1 and S2(P 0.05). There were no significant differences with regard to all above-mentioned indicators between groups S1 and S2 at each time point. 【Conclusion】 Sevoflurane post-conditioning can aggravate 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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【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-conditioning 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 28 th day after injection-operation. Eight rats in each group performed Morris water maze test on 28 th, 35 th and 42 th day after injection-operation and then were sacrificed 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 ineffective search tactics, and the content of Aβ1-42 was significantly increased on 42 th day after injection-operationin groups S1 and S2(P 0.05). There were no significant differences with regard to all above-mentioned indicators between groups S1 and S2 at each time point. 【Conclusion】 Sevoflurane post-conditioning can aggravate the cognitive dysfunction in rats induced by Aβ1-40 and the mechanism is probably related to increasing endogenous Aβ1-42 in hippocampus.
Key concepts: Sevoflurane, Hippocampus, Hippocampal formation, Saline, Conditioning, Morris water navigation task, Anesthesia, Endogeny