Salvianolic Acid A Protects against Acetaminophen-Induced Hepatotoxicity via Regulation of the miR-485-3p/SIRT1 Pathway

被引:7
|
作者
Tang, Fan [1 ]
Wang, Zhecheng [1 ]
Zhou, Junjun [1 ]
Yao, Jihong [1 ]
机构
[1] Dalian Med Univ, Dept Pharmacol, Dalian 116044, Peoples R China
基金
中国国家自然科学基金;
关键词
salvianolic acid A; APAP; miR-485-3p; SIRT1; oxidative stress; inflammation; INDUCED LIVER-INJURY; CIRCULATING MICRORNAS; OXIDATIVE STRESS; ACTIVATION; INFLAMMATION; SIRT1; INHIBITION; BIOMARKERS; APOPTOSIS; OVERDOSE;
D O I
10.3390/antiox12040870
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The vast majority of drug-induced liver injury is mainly attributed to acetaminophen (APAP) overdose. Salvianolic acid A (Sal A), a powerful water-soluble compound obtained from Salvia miltiorrhiza, has been confirmed to exert hepatoprotective effects. However, the beneficial effects and the exact mechanisms of Sal A on APAP-induced hepatotoxicity remain unclear. In this study, APAP-induced liver injury with or without Sal A treatment was examined in vitro and in vivo. The results showed that Sal A could alleviate oxidative stress and inflammation by regulating Sirtuin 1 (SIRT1). Furthermore, miR-485-3p could target SIRT1 after APAP hepatotoxicity and was regulated by Sal A. Importantly, inhibiting miR-485-3p had a hepatoprotective effect similar to that of Sal A on APAP-exposed AML12 cells. These findings suggest that regulating the miR-485-3p/SIRT1 pathway can alleviate oxidative stress and inflammation induced by APAP in the context of Sal A treatment.
引用
收藏
页数:15
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