KMID : 0379520140300010019
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Çѱ¹µ¶¼ºÇÐȸÁö 2014 Volume.30 No. 1 p.19 ~ p.25
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Licochalcone Suppresses LXR¥á-Induced Hepatic Lipogenic Gene Expression through AMPK/Sirt1 Pathway Activation
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Han Jae-Yun
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Abstract
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Licochalcone (LC), a major phenolic retrochalcone from licorice, has anti-inflammatory activity. This study investigated the effects of licochalcone A (LCA) and licochalcone E (LCE) on Liver X receptor-¥á (LXR¥á)-mediated lipogenic gene expression and the molecular mechanisms underlying those effects. LCA and LCE antagonized the ability of LXR¥á agonists (T0901317 or GW3965) to increase sterol regulatory element binding protein-1c (SREBP-1c) expression and thereby inhibited target gene expression (e.g., FAS and ACC) in HepG2 cells. Moreover, treatment with LCA and LCE impaired LXR¥á/RXR¥á-induced CYP7A1-LXRE-luciferase (CYP7A1) transactivation. The AMPK-Sirt1 signaling pathway is an important regulator of energy metabolism and, therefore, a potential therapeutic target for metabolic diseases, including hepatic steatosis. We found here that LCE increased AMPK phosphorylation and Sirt1 expression. We conclude that LC inhibits SREBP-1c-mediated hepatic lipogenesis via activation of the AMPK/Sirt1 signaling pathway.
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KEYWORD
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Licochalcone A, Licochalcone E, Hepatic steatosis, Sterol regulatory element binding protein-1c, Liver X receptor-¥á
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