自噬
安普克
PI3K/AKT/mTOR通路
肝损伤
ULK1
蛋白激酶A
AMP活化蛋白激酶
雷帕霉素的作用靶点
ATG5型
细胞生物学
化学
药理学
激酶
癌症研究
信号转导
生物
生物化学
细胞凋亡
作者
Yu-Xin Yao,Chen-Hao Yao,C. Zhang,Xian-Zhi Peng,Shu Guang Dai,Yu-Jie Yu,Yan-zhi Li,Sheng-Lin Zhang,Yunxia Li
标识
DOI:10.1142/s0192415x2550020x
摘要
. The results demonstrated that CGA could protect the mice and LO2 cells from oxidative stress and liver injury induced by APAP. Regarding mechanisms, CGA activated the AMPK/mTOR/ULK1 pathway, thereby promoting autophagy. This was evidenced by the degradation of p62/SQSTM1 (hereafter referred to as p62), as well as the up-regulation of LC3B, ATG5, and Beclin1. It is worth noting that the aforementioned, CGA-provided beneficial effects were abrogated by pharmacological inhibition of AMPK with Compound C (CC, an AMPK inhibitor). These [Formula: see text] that CGA alleviates oxidative stress and liver injury induced by APAP, which is contingent upon the regulatory effect of CGA on the AMPK/mTOR/ULK1 axis.
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