自噬
肝损伤
细胞凋亡
化学
炎症
细胞生物学
程序性细胞死亡
癌症研究
医学
生物化学
药理学
生物
免疫学
作者
Shuiliang Ruan,Yi Yang,Wenyan Li
出处
期刊:Aging
[Impact Journals LLC]
日期:2022-10-10
卷期号:14 (22): 8970-8981
被引量:13
标识
DOI:10.18632/aging.204330
摘要
This study illustrated the liver protection mechanism of ACP from the perspective of autophagy activation. ACP suppressed the inflammatory injury of KCs, and decreased the cell apoptosis rate. After LTG and LC3 staining, ACP promoted lysosomal production, increased LC3 expression, activated autophagy, and suppressed the expression of NLRP3 and inflammatory factors. Under the electron microscope, ACP accelerated the production of autophagosomes. After simultaneous treatment with 3-MA and ACP, the effect of ACP on resisting KC injury decreased, the expression of NLRP3 was up-regulated, and autophagy was suppressed. As discovered in the mouse model of liver injury, ACP inhibited the ALT and AST levels, promoted the occurrence of autophagy, reduced NLRP3 expression and alleviated liver injury. ACP activates autophagy to induce NLRP3 degradation, thus suppressing inflammatory response in liver injury and exerting the liver protection effect, which is one of the mechanisms of action of ACP.
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