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GANODERMA LUCIDUM SPORE LIPID INDUCES PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR ALPHA ACTIVITY

Authors

  • ZHIYAN HUANG,

    1. Guangzhou Institute of Biomedicine and Health, Guangzhou International Business Incubator, Chinese Academy of Sciences, Guangzhou Science City 510663, China
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  • FANG FANG,

    1. Guangzhou Institute of Biomedicine and Health, Guangzhou International Business Incubator, Chinese Academy of Sciences, Guangzhou Science City 510663, China
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  • CHI-WAI WONG

    Corresponding author
    1. Guangzhou Institute of Biomedicine and Health, Guangzhou International Business Incubator, Chinese Academy of Sciences, Guangzhou Science City 510663, China
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TEL: 86-20-3229-0256; FAX: 86-20-3229-0606; EMAIL: wong_chiwai@gibh.ac.cn

Abstract

ABSTRACT

As a popular medicinal mushroom, Ganoderma lucidum (Leyss. ex Fr.) Karst. (Lingzhi) has been used for centuries in China as food and traditional Chinesemedicine to prevent and treat various diseases. Peroxisome proliferator-activated receptor alpha, gamma and delta (PPARα, PPARγ and PPARδ) are key regulators of energy metabolism. In this study, we presented evidences that G. lucidum spore lipid (GS) dose dependently and preferentially induced the activity of PPARα but not PPARγ and PPARδ. By a gas chromatography–mass spectrometry analysis, we found that GS was rich in unsaturated fatty acids. Additionally, GS induced the expression of PPARa target gene carnitine palmitoyl transferase-1a in human carcinoma HepG2 cells. Collectively, we identified a link between GS and PPARα which suggests that some of the therapeutic effects of GS may bemediated through activating the transcriptional activity of PPARα.

PRACTICAL APPLICATIONS

The induction of CPT-1a by activating PPARα implies that Ganoderma lucidum may also stimulate β-oxidation to reduce liver triglyceride content hence functioning as a hyperlipidemic agent. Ligands of PPARα have also been demonstrated to modulate the immune reaction specifically through suppressing nuclear factor kappa-light-chain-enhancer of activated B cells function. As a consequence of increasing the PPARα function in the liver, GS may improve alcoholic/nonalcoholic fatty liver diseases through suppressing the associated chronic inflammation due to dysregulated lipid homeostasis.

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