7-Chloroarctinone-b as a new selective PPARgamma antagonist potently blocks adipocyte differentiation

Acta Pharmacol Sin. 2009 Sep;30(9):1351-8. doi: 10.1038/aps.2009.113. Epub 2009 Aug 17.

Abstract

Aim: Peroxisome proliferator-activated receptor gamma (PPARgamma) is a therapeutic target for obesity, cancer and diabetes mellitus. In order to develop potent lead compounds for obesity treatment, we screened a natural product library for novel PPARgamma antagonists with inhibitory effects on adipocyte differentiation.

Methods: Surface plasmon resonance (SPR) technology and cell-based transactivation assay were used to screen for PPARgamma antagonists. To investigate the antagonistic mechanism of the active compound, we measured its effect on PPARgamma/RXRalpha heterodimerization and PPARgamma co-activator recruitment using yeast two-hybrid assay, Gal4/UAS cell-based assay and SPR based assay. The 3T3-L1 cell differentiation assay was used to evaluate the effect of the active compound on adipocyte differentiation.

Results: A new thiophene-acetylene type of natural product, 7-chloroarctinone-b (CAB), isolated from the roots of Rhaponticum uniflorum, was discovered as a novel PPARgamma antagonist capable of inhibiting rosiglitazone-induced PPARgamma transcriptional activity. SPR analysis suggested that CAB bound tightly to PPARgamma and considerably antagonized the potent PPARgamma agonist rosiglitazone-stimulated PPARgamma-LBD/RXRalpha-LBD binding. Gal4/UAS and yeast two-hybrid assays were used to evaluate the antagonistic activity of CAB on rosiglitazone-induced recruitment of the coactivator for PPARgamma. CAB could efficiently antagonize both hormone and rosiglitazone-induced adipocyte differentiation in cell culture.

Conclusion: CAB shows antagonistic activity to PPARgamma and can block the adipocyte differentiation, indicating it may be of potential use as a lead therapeutic compound for obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells / drug effects
  • Adipocytes / drug effects*
  • Adipogenesis / drug effects
  • Animals
  • Cell Differentiation / drug effects
  • Dimerization
  • Humans
  • Mice
  • PPAR gamma / antagonists & inhibitors*
  • Surface Plasmon Resonance
  • Thiophenes / pharmacology*
  • Transcriptional Activation / drug effects
  • Two-Hybrid System Techniques

Substances

  • 7-chloroarctinone-b
  • PPAR gamma
  • Thiophenes