Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 142, Issue -, Pages -Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2021.112092
Keywords
Angelicae sinensis radix; High-fat diet; Metabolic dysfunction-associated fatty liver; Mitochondria; Polygonati Rhizoma; n-oxidation
Funding
- National Natural Science Foundation of China [82060707, 81960710]
- Application and Basis Research Project of Yunnan, China [2019FF002-061, 2017FF117-013]
- Key Research and Development Program of Yunnan, China [2019IB009]
- Young and Middle-aged Academic and Technological Leader of Yunnan, China [202005AC160059]
- National Science Foundation for Distinguished Young Scholars of Yunnan, China [202001AV070007]
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JHP alleviates HFD-induced MAFLD through the protection of mitochondrial function, as shown by the results of decreased levels of total cholesterol, triglyceride, LDL-C, ALT, and AST, and increased HDL-C, as well as regulation of oxidative stress and fatty acid metabolism.
Background: Metabolic dysfunction-associated fatty liver disease (MAFLD) is a common global chronic liver disease. Jiuzhuan Huangjing Pills (JHP) have been used for the treatment of human disease for over a thousand years, but their efficacy and underlying mechanism(s) of action against MAFLD are unknown. We investigated the alleviating effects of JHP on high-fat diet (HFD)-induced MAFLD. Methods: In vitro and in vivo methods were used to evaluate the effects of JHP on MAFLD. L02 adipocyte models were induced by fat emulsion and adipocytes were treated with JHP for 24 h. MAFLD rat models were induced by HFD-feeding and were intragastrically administered JHP for 12 weeks. Changes in fat accumulation, L02 cell damage, body weight, food intake, histological parameters, organ indexes, biochemical parameters, and mitochondrial indicators including ultrastructure, oxidative stress, energy metabolism, and fatty acid metabolism were investigated. Results: JHP attenuated the increase in levels of total cholesterol, triglyceride, low density lipoprotein cholesterol, alanine transaminase, and aspartate transaminase levels, and significantly increased high density lipoprotein cholesterol. JHP up-regulated levels of glutathione (GSH) and superoxide dismutase (SOD), and down-regulated malondialdehyde (MDA). JHP afforded protection to the mitochondrial ultrastructure, and inhibited the HFDinduced increase in MDA and the reduction of SOD, GSH, ATP synthase, and complex I and II, in liver mitochondria. JHP regulated the expression of n-oxidation genes, including acyl-CoA dehydrogenase, cyl-CoA dehydrogenase long chain, carnitine palmitoyltransferase 1A, carnitine palmitoyltransferase 1B, peroxisomal proliferator-activated receptor-gamma coactivator-1 alpha and peroxide proliferator activated receptor alpha. Conclusion: JHP alleviates HFD-induced MAFLD through the protection of mitochondrial function.
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