The improvement provided by physcion on non-alcoholic fatty liver disease in mice
10.16438/j.0513-4870.2023-1158
- VernacularTitle:大黄素甲醚改善小鼠非酒精性脂肪性肝病的研究
- Author:
Jin-yu ZHANG
1
;
Shao-bo ZHANG
1
;
Hong XU
1
;
Hao OUYANG
1
,
2
;
Li-li JI
1
Author Information
1. The MOE Key Laboratory for Standardization of Chinese Medicines, the SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines, Shanghai Key Laboratory of Compound Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
2. Department of Hepatology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
- Publication Type:Research Article
- Keywords:
physcion;
non-alcoholic fatty liver disease;
carnitine palmitoyltransferase 1A;
italic>β-oxidation;
mitochondrial damage
- From:
Acta Pharmaceutica Sinica
2024;59(4):939-947
- CountryChina
- Language:Chinese
-
Abstract:
Physcion (PHY) is an anthraquinone compound derived from traditional Chinese medicine such as Rhei Radix et Rhizoma. The aim of this study is to investigate the improvement of PHY on non-alcoholic fatty liver disease (NAFLD) and its underlying mechanism. NAFLD was induced in mice by feeding with the methionine- and choline-deficient diet (MCD) for 6 weeks. This experiment was approved by the Experimental Animal Ethics Committee of Shanghai University of Traditional Chinese Medicine (approval number: PZSHUTCM190705019). The results displayed that PHY (5 and 20 mg·kg-1) reversed liver damage, reduced hepatic lipid accumulation and decreased the elevated NAFLD activity score (NAS) in MCD-fed NAFLD mice. Results from Western blot and enzyme activity demonstrated that PHY could enhance the protein expression and enzyme activity of carnitine palmitoyltransferase 1A (CPT1A) in the liver and L-02 cells, but it did not affect Cpt1a mRNA expression. Immunofluorescence results indicated that PHY (10 and 25 μmol·L-1) could reduce the mitochondrial injury induced by non-esterified fatty acids (NEFA) in L-02 cells. Results from seahorse assay showed that PHY could enhance mitochondrial basic respiration, maximal respiration, ATP synthesis and reserve respiration in L-02 cells treated with NEFA, but had no effect on mitochondrial proton leakage. In summary, PHY reversed mitochondrial damage and enhanced fatty acid β-oxidation, thereby reducing hepatic steatosis and improving NAFLD.
