Blockade of lipid accumulation by silibinin in adipocytes and zebrafish

Hyung Joo Suh, So Young Cho, Eun Young Kim, Hyeon Son Choi

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Silibinin is a compound present mainly in milk thistle. In this study, we investigated the mechanism by which silibinin suppresses adipogenesis of 3T3-L1 cells, and evaluated the anti-adipogenic effect of silibinin in zebrafish. Silibinin reduced lipid accumulation by downregulating adipogenic factors, such as, peroxisome proliferator-activated receptor γ (PPARγ), CCAAT-enhancer binding protein α (C/EBPα), and fatty acid-binding protein 4 (FABP4). The reduction of these adipogenic protein levels was associated with the regulation of early adipogenic factors, such as, C/EBPβ and Krüppel-like factor 2 (KLF2), and was reflected in downregulation of lipid synthetic enzymes. Silibinin arrested cells in the G0/G1 phase of the cell cycle, accompanied by downregulation of cyclins and upregulation of p27, a cell cycle inhibitor. These results correlated with the finding of deactivation of extracellular signal-regulated kinase (ERK) and AKT, a serine/threonine-specific kinase. In addition, silibinin activated AMP-activated protein kinase α (AMPKα) to inhibit fatty acid synthesis. As observed in 3T3-L1 cells, silibinin inhibited lipid accumulation in zebrafish with the reduction of adipogenic factors and triglyceride levels. Our data revealed that silibinin inhibited lipid accumulation in 3T3-L1 cells and zebrafish, and this inhibitory effect was associated with abrogation of early adipogenesis via regulation of cell cycle and AMPKα signaling.

Original languageEnglish
Pages (from-to)53-62
Number of pages10
JournalChemico-Biological Interactions
Volume227
DOIs
Publication statusPublished - 2015 Feb 5

Keywords

  • 3T3-L1
  • Adipogenesis
  • AMPKα
  • Cell cycle arrest
  • Silibinin
  • Zebrafish

ASJC Scopus subject areas

  • Toxicology

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