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归芪多糖延缓细胞衰老的分子作用机制
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引用本文:罗阿苗,蒲秀瑛 ,张凯丽,田昌义,陈 博,苏 慧,柴鹏弟,夏晓雨.归芪多糖延缓细胞衰老的分子作用机制[J].西北农业学报,2020,30(10):1583~1592
DOI:10.7606/j.issn.1004-1389.2020.10.016
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作者单位
罗阿苗,蒲秀瑛 ,张凯丽,田昌义,陈 博,苏 慧,柴鹏弟,夏晓雨 (兰州理工大学 生命科学与工程学院甘肃省中藏药筛选评价及深加工重点实验室兰州 730050) 
基金项目:国家自然科学基金(81860257);甘肃省高校中藏药筛选评价及深加工重点实验室开放基金(20180808)。
中文摘要:以SIRT1和线粒体为切入点,采用分子生物学技术以及多种线粒体分析技术,深入探讨SIRT1和线粒体在衰老细胞中的作用,揭示归芪多糖延缓细胞衰老的分子作用机制。结果表明,AAP显著降低细胞的衰老程度并提高细胞活力,而Ex527阻断AAP的作用。同时,发现AAP增强细胞内SIRT1和CyclinD1的表达,降低p53的表达水平,在Ex527组中未观察到类似的逆转作用。线粒体分析结果显示,AAP可显著降低细胞内的活性氧水平,降低线粒体膜电位,减轻线粒体肿胀程度和增加线粒体内ATP含量,而Ex527的预处理消除这些作用。基于上述结果,推测AAP可能通过信号通路p53/p16和CyclinD/CDK4来改善线粒体功能,从而达到延缓衰老的作用,且这些作用与SIRT1密切相关。
中文关键词:归芪多糖  细胞衰老  SIRT1  线粒体  分子机制
 
Molecular Mechanism of Guiqi Polysaccharides in Delaying Cell Senescence
Abstract:This study aims to investigate the role of SIRT1 and mitochondria in the aging cells and the molecular mechanism of AAP in delaying the senescence of WI-38 cells. Using SIRT1 and mitochondria as entry points,molecular biology and various mitochondrial analysis techniques were adopted to deeply explore the role of SIRT1 and mitochondria in senescent cells,the molecular mechanism of Guiqi polysaccharides for delaying cell aging was revealed. The experimental results showed that AAP significantly reduced the degree of cell senescence and increased the cell viability while Ex527 reversed the effect of AAP. Meanwhile,we found that AAP enhanced the expressions of SIRT1 and CyclinD1,and decreased the level of p53,but similar reversed effect was not observed in the Ex527 group. Finally,AAP also significantly decreased intracellular reactive oxygen species,sharply reduced mitochondrial membrane potential and the degree of membrane swelling,and evidently increased mitochondrial ATP levels,while Ex527 blocked these effects. In conclusion,it is speculated that AAP may play a role in delaying cell aging by improving mitochondrial function through signal pathways such as p53/p16 and CyclinD/CDK4,and these effects are closely related to SIRT1.
keywords:Guiqi polysaccharide(AAP)  Cell senescence  SIRT1  Mitochondria  Molecular mechanism
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