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通过调节NAD+代谢和促进IDO2/QPRT表达来延缓肝细胞衰老

Chen Guo^1,2, Ming-Xia Wu², Ze-Peng Zhang^1,2

¹Research Center of Traditional Chinese Medicine, The Affiliated Hospital of Changchun University of Chinese Medicine, Jilin, 130021, China.

Journal of ginseng research

|August 22, 2025

概括

通过促进尼古丁胺氨基二核酸 (NAD+) 代谢,Panax人参的总体人参酸 (GS) 改善了老年小鼠的健康. 丁胺Rb2通过IDO2/ QPRT途径特别增强线粒体功能并延缓细胞衰老.

科学领域:

老年学
分子生物学
代谢学

背景情况:

尼古丁胺氨基二核酸 (NAD+) 稳定对于衰老过程至关重要.
针对NAD+代谢提供了延迟衰老干预的潜在策略.
帕纳克斯人参中的活性化合物金赛诺化物具有延迟衰老的作用,但它们对NAD+代谢的机制尚不清楚.

研究的目的:

调查总体人参酸 (GS) 对NAD+代谢和衰老的影响.
阐明基因酸中介抗衰老作用的分子机制.
确定参与调节NAD+平衡的特定人参和途径.

主要方法:

使用行为测试,心脏超声波,生化分析和组织学来评估老年小鼠.
液体染色体质谱 (LC-MS) 量化了NAD+代谢物.
通过与衰老相关的分泌表型 (SASP),NAD+水平和线粒体功能来评估细胞衰老.
在体外研究中,使用小鼠肝细胞 (AML12) 选活跃的金赛诺化物和IDO2倒置,以验证机制.

主要成果:

在老年小鼠中,GS的使用改善了身体健康,认知功能和器官健康.
在多个器官中改善了与年龄相关的病理变化.
主要影响肝脏中的NAD+新生合成途径.
鉴定出银酸Rb2 (Rb2) 能够促进NAD+代谢,增强线粒体功能,并减少AML12细胞的衰老.
通过GS和Rb2扭转了IDO2的淘汰效应,证实了它们的作用.

结论:

总体人参酸 (GS),特别是人参酸Rb2 (Rb2) 增强线粒体功能,并延缓肝细胞衰老.
通过调节依赖于IDO2/ QPRT的NAD+新生生物合成途径来促进抗衰老作用.
这项研究通过NAD+新陈代谢调节,为人参酸在抗衰老中的作用提供了新的见解.

关键词:

年龄增长新生生物合成途径基因化物Rb2 尼古丁胺二核酸总体的化物

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