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基酸通过AMPK/mTOR/ULK1-介导的自激活来改善乙氨基诱导的肝损伤

Yu-Xin Yao^1,2,3, Chen-Hao Yao^1,2,3, Chao-Yang Zhang^1,2,3

¹State Key Laboratory of Southwestern Chinese Medicine Resources, Chengdu 611137, China.

The American journal of Chinese medicine

|March 27, 2025

概括

酸 (CGA) 通过激活AMPK/mTOR/ULK1通路,促进自,从而防止乙氨基诱导的肝损伤 (AILI). 这种机制减轻氧化应激和肝损伤,为AILI提供治疗策略.

科学领域:

肝病学肝病学是一种肝病学.
细胞生物学细胞生物学
药理学药理学是指药理学的学科.

背景情况:

乙氨基 (APAP) 诱导的肝损伤 (AILI) 是急性肝衰竭的主要原因.
自,特别是AMP激活蛋白激酶 (AMPK) /乳动物目标的拉巴胺素 (mTOR) /unc-51-like激酶1 (ULK1) 途径,在APAP肝毒性中起着至关重要的作用.
这种途径的药理激活是AILI的一种有前途的治疗策略.

研究的目的:

调查酸 (CGA) 对AILI的保护作用.
阐明CGA在AILI中调节自的基本机制.
在体外和体外模型中探索CGA对AMPK/mTOR/ULK1通路的影响.

主要方法:

向小鼠和LO2细胞给予CGA,这些小鼠和LO2细胞遭受了APAP诱导的肝损伤.
评估肝损伤标志物和氧化应激水平.
分析了与自相关的蛋白质表达 (p62,LC3B,ATG5,Beclin1) 和通路激活 (AMPK/mTOR/ULK1).
使用化合物C (CC) 抑制AMPK并评估其对CGA保护机制的影响.

主要成果:

在小鼠和LO2细胞中,CGA对APAP诱导的肝损伤和氧化应激产生显著的保护.
CGA治疗促进了自,由p62降解和LC3B,ATG5和Beclin1.1的升调证明.
CGA激活了AMPK/mTOR/ULK1的信号通路.
化合物C对AMPK的抑制取消了CGA的保护作用,证实了该途径的重要作用.

结论:

CGA有效地减轻了APAP诱导的肝损伤和氧化应激.
CGA通过激活AMPK/mTOR/ULK1通路来发挥其保护作用,从而促进自.
这些发现强调了CGA作为AILI的潜在治疗剂,取决于其对AMPK/mTOR/ULK1轴的调节作用.

关键词:

在 AMPK/mTOR/ULK1 信号传输中.由APAP引起的肝损伤自自是一种自的过程.基酸是一种基酸.

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