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异黄酮苷元对衰老加速小鼠认知功能影响的作用机制。

Mechanism of isoflavone aglycone's effect on cognitive performance of senescence-accelerated mice.

机构信息

Jinan University, 601 Huang Pu Road, Guangzhou, Guangdong 510632, PR China.

出版信息

Brain Cogn. 2011 Jun;76(1):206-10. doi: 10.1016/j.bandc.2010.10.008. Epub 2011 Apr 3.

DOI:10.1016/j.bandc.2010.10.008
PMID:21463916
Abstract

This study investigated the effect of isoflavone aglycone (IA) on the learning and memory performance of senescence-accelerated mice, and explored its neural protective mechanism. Results showed that SAM-P/8 senescence-accelerated mice treated with IA performed significantly better in the Y-maze cognitive test than the no treatment control (P<0.05). The cortex AchE activity, serum SOD and GSH-Px activities were notably higher (P<0.05). MDA concentration and the β-secretase activity in the hippocampal tissue were both lower (P<0.05). Additionally, the number of hippocampal neurons was increased and cell morphology was significantly improved. Data suggested that IA could indirectly increase concentration of the cholinergic neural transmitter Ach through regulation of AchE, therefore improving the central cholinergic function and enhancing the learning and memory ability. By reducing the β-secretase activity, IA could decrease the formation and deposition of insoluble Adebris, relieve the resulted toxicity and damage to neurons, and thereby effectively protect the nervous system.

摘要

本研究探讨了异黄酮苷元(IA)对快速老化小鼠学习记忆能力的影响,并探讨了其神经保护机制。结果表明,IA 处理的 SAM-P/8 快速老化小鼠在 Y 迷宫认知测试中的表现明显优于未处理对照组(P<0.05)。大脑皮质 AchE 活性、血清 SOD 和 GSH-Px 活性显著升高(P<0.05)。海马组织 MDA 浓度和β-分泌酶活性均降低(P<0.05)。此外,海马神经元数量增加,细胞形态明显改善。数据表明,IA 可以通过调节 AchE 间接增加胆碱能神经递质 Ach 的浓度,从而改善中枢胆碱能功能,增强学习记忆能力。IA 通过降低β-分泌酶活性,减少不溶性 Adebris 的形成和沉积,减轻其对神经元的毒性和损伤,从而有效保护神经系统。

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