Salvianolic acid A activates AMPK and SIRT1 to reduce palmitic acid-induced lipotoxicity in hepatocyte
10.12092/j.issn.1009-2501.2021.03.001
- Author:
Fangqing ZHAO
1
;
Wenwen YANG
1
;
Yujie YIN
1
;
Xiaobing DOU
1
;
Bin ZHANG
2
;
Bangcai WANG
2
;
Xiaobing DOU
3
;
Songtao LI
3
;
Songtao LI
4
;
Linwensi ZHU
5
Author Information
1. School of Life Sciences, Zhejiang University of Traditional Chinese Medicine
2. Department of Gastroenterology, Ningbo Traditional Chinese Medicine Hospital
3. Institute of Molecular Medicine, Zhejiang Chinese Medical University
4. School of Basic Medicine & Public Health, Zhejiang Chinese Medical University
5. Department of Gastroenterology, The First Affiliated Hospital of Zhejiang University of Traditional Chinese Medicine
- Publication Type:Journal Article
- Keywords:
AMP-activated protein kinase;
Lipotoxicity;
Salvianolic acid A;
Silent information regulator 1
- From:
Chinese Journal of Clinical Pharmacology and Therapeutics
2021;26(3):241-249
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the protective affect of salvianolic acid A on palmitic acid-induced lipotoxicity in hepatocyte and its potential molecular mechanism. METHODS: The lipotoxicity model of AML12 hepatocytes induced by PA was established. Different concentrations of Sal A (20, 40, 80, 120 μmol/L) were intervened. The hepatocyte injury was detected by the Lactate dehydrogenase (LDH) method, the intracellular triglyceride (TG) content was detected by enzyme assay and the lipid droplets were observed by Bodipy staining, cell viability was detected by MTT, Intracellular reactive oxygen species (ROS) were detected by 2'eci'- dichlorofluorescein diacetate (DCFH-DA) and fluorescence microscope. Mitochondrial membrane potential was detected by rhodamine 123 and fluorescence microscope. The expression of phosphorylation of AMP-activated protein kinase (AMPK) protein and silent information regulator 1 (SIRT1) protein were observed by Western blot. RESULTS: Model of hepatocyte lipotoxicity was established after intervented for 12 h in vitro with PA (0.5 mmol/L). Different concentrations of Sal A could significantly reduce the lipid deposition and hepatocytes injury induced by PA (P<0.05), and the protective effect was dose-dependent. Secondly, Sal A could significantly improve cell mitochondrial membrane potential (P<0.01) and abate the ROS level of hepatocytes induced by PA (P<0.01). In addition, PA could significantly inhibit AMPK and SIRT1 protein expression (P<0.05). Salvianolic acid A can significantly up-regulate SIRT1 and AMPK protein expression (P<0.05). CONCLUSION: Sal A improves PA induced lipotoxicity in hepatocyte, AMPK and SIRT1 may be a potential molecular target.
