首页> 美国卫生研究院文献>Oxidative Medicine and Cellular Longevity >Ginsenoside Rg1 Ameliorates Behavioral Abnormalities and Modulates the Hippocampal Proteomic Change in Triple Transgenic Mice of Alzheimers Disease
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Ginsenoside Rg1 Ameliorates Behavioral Abnormalities and Modulates the Hippocampal Proteomic Change in Triple Transgenic Mice of Alzheimers Disease

机译:人参皂苷Rg1改善行为异常并调节阿尔茨海默氏病三重转基因小鼠的海马蛋白质组学变化。

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摘要

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases, so far, there are no effective measures to prevent and cure this deadly condition. Ginsenoside Rg1 (Rg1) was shown to improve behavioral abnormalities in AD; however, the potential mechanisms remain unclear. In this study, we pretreated 7-month-old 3xTg-AD mice for 6 weeks with Rg1 and evaluated the effects of Rg1 on the behaviors and the protein expression of hippocampal tissues. The behavioral tests showed that Rg1 could improve the memory impairment and ameliorate the depression-like behaviors of 3xTg-AD mice. Proteomic results revealed a total of 28 differentially expressed hippocampal proteins between Rg1-treated and nontreated 3xTg-AD mice. Among these proteins, complexin-2 (CPLX2), synapsin-2 (SYN2), and synaptosomal-associated protein 25 (SNP25) were significantly downregulated in the hippocampus of 3xTg-AD mice compared with the WT mice, and the treatment of Rg1 modulated the expression of CPLX2 and SNP25 in the hippocampus of 3xTg-AD mice. The expression of CPLX2, SYN2, and SNP25 was further validated by Western blot analysis. Taken together, we concluded that Rg1 could be a potential candidate drug to improve the behavioral deficits in AD via modulating the expression of the proteins (i.e., CPLX2, SYN2, and SNP25).
机译:阿尔茨海默氏病(AD)是最常见的神经退行性疾病之一,到目前为止,尚无有效的方法来预防和治愈这种致命疾病。人参皂苷Rg1(Rg1)被证明可以改善AD的行为异常。但是,潜在的机制仍不清楚。在这项研究中,我们用Rg1预处理了7个月大的3xTg-AD小鼠6周,并评估了Rg1对行为和海马组织蛋白质表达的影响。行为测试表明,Rg1可以改善3xTg-AD小鼠的记忆障碍并改善抑郁样行为。蛋白质组学结果显示,在Rg1治疗和未治疗的3xTg-AD小鼠之间共有28种差异表达的海马蛋白。在这些蛋白质中,与WT小鼠相比,3xTg-AD小鼠海马中的complexin-2(CPLX2),synapsin-2(SYN2)和突触体相关蛋白25(SNP25)显着下调,并且对Rg1的治疗进行了调节CPLX2和SNP25在3xTg-AD小鼠海马中的表达通过蛋白质印迹分析进一步验证了CPLX2,SYN2和SNP25的表达。两者合计,我们得出结论,Rg1可能是通过调节蛋白质(即CPLX2,SYN2和SNP25)的表达来改善AD行为缺陷的潜在候选药物。

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