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Toxicol Res. 2014 Mar;30(1):19-25.

Licochalcone Suppresses LXRα-Induced Hepatic Lipogenic Gene Expression through AMPK/Sirt1 Pathway Activation.

Author information

1
College of Pharmacy, Chosun University, Gwangju, Korea.
2
College of Pharmacy, Mokpo National University, Muan, Jeonnam, Korea.
3
College of Pharmacy and Research Institute of Drug Development, Chonnam National University, Gwangju, Korea.

Abstract

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-α (LXRα)-mediated lipogenic gene expression and the molecular mechanisms underlying those effects. LCA and LCE antagonized the ability of LXRα 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 LXRα/RXRα-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.

KEYWORDS:

Hepatic steatosis; Licochalcone A; Licochalcone E; Liver X receptor-α; Sterol regulatory element binding protein-1c

PMID:
24795795
PMCID:
PMC4007039
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