Long-term ginsenoside Rg1 supplementation improves age-related cognitive decline by promoting synaptic plasticity associated protein expression in C57BL/6J mice

YangL.; ZhangJ.; ZhengK.; ShenH.; ChenX.

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Long-term ginsenoside Rg1 supplementation improves age-related cognitive decline by promoting synaptic plasticity associated protein expression in C57BL/6J mice

机译：长期人参皂甙Rg1补充通过促进C57BL / 6J小鼠突触可塑性相关蛋白的表达来改善与年龄有关的认知下降

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In aging individuals, age-related cognitive decline is the most common cause of memory impairment. Among the remedies, ginsenoside Rg1, a major active component of ginseng, is often recommended for its antiaging effects. However, its role in improving cognitive decline during normal aging remains unknown and its molecular mechanism partially understood. This study employed a scheme of Rg1 supplementation for female C57BL/6J mice, which started at the age of 12 months and ended at 24 months, to investigate the effects of Rg1 supplementation on the cognitive performance. We found that Rg1 supplementation improved the performance of aged mice in behavior test and significantly upregulated the expression of synaptic plasticity-associated proteins in hippocampus, including synaptophysin, N-methyl-d-aspartate receptor subunit 1, postsynaptic density-95, and calcium/calmodulin-dependent protein kinase II alpha, via promoting mammalian target of rapamycin pathway activation. These data provide further support for Rg1 treatment of cognitive degeneration during aging.

机译：在衰老的个体中，与年龄相关的认知能力下降是记忆障碍的最常见原因。在这些疗法中，人参皂苷Rg1是人参的主要活性成分，通常被建议具有抗衰老作用。然而，其在正常衰老过程中改善认知能力下降的作用仍然未知，其分子机制也被部分理解。这项研究采用了CgBL / 6J雌性小鼠补充Rg1的方案，该方案始于12个月大，结束于24个月，以研究补充Rg1对认知能力的影响。我们发现补充Rg1可以改善行为测试中衰老小鼠的性能，并显着上调海马中突触可塑性相关蛋白的表达，包括突触素，N-甲基-d-天冬氨酸受体亚基1，突触后密度95和钙/钙调蛋白依赖性蛋白激酶IIα，通过促进哺乳动物雷帕霉素途径活化的靶标。这些数据为Rg1治疗衰老过程中的认知变性提供了进一步的支持。

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《The journals of gerontology.Series A. Biological sciences and medical sciences》 |2014年第3期|共13页
作者
YangL.; ZhangJ.; ZhengK.; ShenH.; ChenX.;
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正文语种 eng
中图分类老年病学;
关键词
Aging; Cognition; Ginsenoside; MTOR; Synapse;

机译：衰老;认知;人参皂苷;MTOR;突触;

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1. Long-term ginsenoside Rg1 supplementation improves age-related cognitive decline by promoting synaptic plasticity associated protein expression in C57BL/6J mice [J] . YangL., ZhangJ., ZhengK., The journals of gerontology.Series A. Biological sciences and medical sciences . 2014,第3期

机译：长期人参皂甙Rg1补充通过促进C57BL / 6J小鼠突触可塑性相关蛋白的表达来改善与年龄有关的认知下降
2. LONG-TERM GINSENOSIDE ADMINISTRATION PREVENTS MEMORY LOSS IN AGED FEMALE C57BL/6J MICE BY MODULATING THE REDOX STATUS AND UP-REGULATING THE PLASTICITY-RELATED PROTEINS IN HIPPOCAMPUS [J] . H. F. ZHAO, Q. Ll AND Y. Ll Neuroscience: An International Journal under the Editorial Direction of IBRO . 2011,第Null期

机译：通过调节氧化还原状态和Up-Consemate在海马中的可塑性相关蛋白质中，长期人参皂苷给药可防止老年女性C57BL / 6J小鼠中的记忆丧失
3. Sex-differences in age-related cognitive decline in C57BL/6J mice associated with increased brain microtubule-associated protein 2 and synaptophysin immunoreactivity. [J] . Benice TS, Rizk A, Kohama S, Neuroscience: An International Journal under the Editorial Direction of IBRO . 2006,第2期

机译：C57BL / 6J小鼠与年龄相关的认知能力下降的性别差异与脑微管相关蛋白2的增加和突触素免疫反应性有关。
4. Benzothiazole Derivative Accelerates Excretion of Total Sterols in Long-Term High Fat Fed C57BL/6J Mice [C] . Yue Yu, Heng Jiang, Junli Ao, International Conference on Materials chemistry and environmental protection . 2015

机译：苯并噻唑衍生物在长期高脂肪喂养C57BL / 6J小鼠中加速了总甾醇的排泄
5. The influence of transferred ubxiap on the progression of age-related hearing loss in C57BL/6J mice. [D] . Menchenton, Trevor Wesley. 2008

机译：转移的ubxiap对C57BL / 6J小鼠与年龄有关的听力损失的进展的影响。
6. Hippocampal dysregulation of synaptic plasticity-associated proteins with age-related cognitive decline [O] . Heather D. VanGuilder, Julie A. Farley, Han Yan, -1

机译：突触塑性相关蛋白的海马失呼患者与年龄相关的认知下降
7. Long-term Ginsenoside Rg1 Supplementation Improves Age-Related Cognitive Decline by Promoting Synaptic Plasticity Associated Protein Expression in C57BL/6J Mice [O] . L. Yang, J. Zhang, K. Zheng, 2013

机译：通过在C57BL / 6J小鼠中促进突触可塑性相关蛋白表达，长期人参皂苷RG1补充提高年龄相关的认知下降

Long-term ginsenoside Rg1 supplementation improves age-related cognitive decline by promoting synaptic plasticity associated protein expression in C57BL/6J mice

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