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International Journal of Medicinal Mushrooms
Fator do impacto: 1.423 FI de cinco anos: 1.525 SJR: 0.431 SNIP: 0.716 CiteScore™: 2.6

ISSN Imprimir: 1521-9437
ISSN On-line: 1940-4344

Volumes:
Volume 22, 2020 Volume 21, 2019 Volume 20, 2018 Volume 19, 2017 Volume 18, 2016 Volume 17, 2015 Volume 16, 2014 Volume 15, 2013 Volume 14, 2012 Volume 13, 2011 Volume 12, 2010 Volume 11, 2009 Volume 10, 2008 Volume 9, 2007 Volume 8, 2006 Volume 7, 2005 Volume 6, 2004 Volume 5, 2003 Volume 4, 2002 Volume 3, 2001 Volume 2, 2000 Volume 1, 1999

International Journal of Medicinal Mushrooms

DOI: 10.1615/IntJMedMushrooms.2017024589
pages 1101-1111

Lipid-Modulating Effect of Black Lingzhi Medicinal Mushroom, Amauroderma rugosum (Agaricomycetes), on Oleate-Induced Human Hepatocellular Liver Carcinoma Cells

Chan Kam Seng
Mushroom Research Centre & Institute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur, Malaysia
Noorlidah Abdullah
Mushroom Research Centre, Institute of Biological Sciences, Faculty of Science, University of Malaya, 50603 Kuala Lumpur, Malaysia
Norhaniza Aminudin
Mushroom Research Centre, Institute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur, Malaysia

RESUMO

Dyslipidemia is the key precursor of atherosclerotic cardiovascular disease. The aim of this study was to investigate the lipid-modifying potential of organic solvent–partitioned extracts from fruiting bodies of Amauroderma rugosum in vitro using oleate-induced human hepatocellular liver carcinoma (HepG2) cells. Our results demonstrated that oleate-induced HepG2 cells treated with ethyl acetate (EA) extract greatly decreased intracellular and secreted total triglyceride (TG) and total cholesterol (TC) compared with other extracts. Further investigation of cellular expression of selected apolipoproteins also revealed that oleate-induced HepG2 cells treated with the EA extract best attenuated the apolipoprotein (Apo) profile by downregulating ApoB-100 and ApoE while upregulating ApoA1. Because both ApoB-100 and ApoE are key components of low-density lipoprotein (LDL) and very LDL (VLDL), which are recognized as "bad cholesterol," this result indicates that treatment with the EA extract inhibited LDL and VLDL production in oleate-induced HepG2 cells. On the other hand, increasing ApoA1 evidence shows antiatherogenic benefits to increasing ApoA1, the key component of high-density lipoprotein (HDL), particularly in relation to its role in promoting reverse cholesterol transport and preventing LDL oxidation; this indicates that the EA extract upregulated the production of HDL ("good cholesterol"). Hence, the EA extract is a good source of lipid-ameliorating agents in the management of dyslipidemia.


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