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

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

DOI:
10.1093/gerona/glt091
复制
发表时间:
2014-03
期刊:
The journals of gerontology. Series A, Biological sciences and medical sciences
影响因子:
--
通讯作者:
Lu-meng Yang;Jing Zhang;Kunmu Zheng;Hui Shen;Xiaochun Chen
Lu-meng Yang;Jing Zhang;Kunmu Zheng;Hui Shen;Xiaochun Chen
中科院分区:
其他
文献类型:
--
作者:
Lu-meng Yang;Jing Zhang;Kunmu Zheng;Hui Shen;Xiaochun Chen

文献摘要

被引文献

相似文献

在老年人中,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(人参的主要活性成分)因其抗衰老作用而经常被推荐。然而,其在改善正常衰老过程中认知能力下降的作用仍不清楚,其分子机制也部分了解。本研究采用雌性C57BL/6J小鼠的Rg1补充方案,从12月龄开始至24月龄结束,以研究补充Rg1对认知表现的影响。我们发现补充Rg1可改善老年小鼠在行为测试中的表现,并通过促进哺乳动物雷帕霉素靶标显着上调海马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II α 通路激活。这些数据为Rg​​1治疗衰老过程中认知退化提供了进一步的支持。
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.