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International Journal of Medicinal Mushrooms
Импакт фактор: 1.423 5-летний Импакт фактор: 1.525 SJR: 0.431 SNIP: 0.661 CiteScore™: 1.38

ISSN Печать: 1521-9437
ISSN Онлайн: 1940-4344

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

Краткое описание

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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