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Ruoqing Guan^1,2, Zhaoyun Xue^1,2, Kaikun Huang^3,4

¹National and Local United Engineering Lab of Druggability and New Drugs Evaluation, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.

Pharmaceuticals (Basel, Switzerland)

|August 28, 2025

概括

通过抑制mTOR信号传递和增强线粒体功能,阿尔法质酸盐 (AKG) 降低了氧化应激诱导的神经元衰老. 这种代谢干预对与年龄相关的神经退行性疾病具有前景.

科学领域:

神经科学
生物化学
老年学

背景情况:

氧化压力是神经退化和大脑衰老的关键驱动因素.
作为三酸循环的中间体,阿尔法谷酸 (AKG) 具有长寿和抗氧化应激的潜力.
AKG在神经元衰老中的作用及其在衰老过程中与mTOR信号的相互作用尚不清楚.

研究的目的:

研究AKG对氧化应激诱导的神经衰老的神经保护作用.
探索AKG对神经元衰老中的mTOR信号通路的影响.
评估AKG作为与年龄相关的神经退行性疾病的潜在治疗方法.

主要方法:

在HT22细胞中利用H2O2诱导的衰老和D-银糖诱导的大脑衰老的小鼠模型.
评估了衰老标志物,线粒体功能,ROS水平和抗氧化剂标志物.
采用蛋白质基因分析和西方抹杀来分析AKG响应信号通路,特别是mTOR.

主要成果:

在试验室中,AKG缓解了细胞衰老,提高了细胞活力,减少了氧化应激,并恢复了线粒体功能.
在体内,AKG改善了老年小鼠的认知和运动功能,并减少了脑氧化损伤.
AKG抑制了mTOR酸化,激活了ULK1,增强了抗氧化活性,并改善了氧化还原平衡.

结论:

AKG通过抑制mTOR通路并增强线粒体和抗氧化功能来缓解氧化压力诱导的神经衰老.
这些发现将AKG作为对抗与年龄相关的神经退行性疾病的有前途的代谢干预措施.

关键词:

D-银糖 H2O2 其他一个TCA 阿尔法基酸盐大脑衰老在 mTOR 蛋白质的

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