Platycodin D inhibits adipogenesis of 3T3‐L1 cells by modulating kruppel‐like factor 2 and peroxisome proliferator‐activated receptor γ

In this study, platycodin D was found to inhibit intracellular triglyceride accumulation in 3T3-L1 cells with an IC(50) of 7.1 microM. The expression levels of genes involved in lipid metabolism such as fatty-acid-binding protein 4 and lipoprotein lipase were significantly downregulated following treatment with platycodin D. Treatment with platycodin D also resulted in a reduction of Peroxisome proliferator-activated receptor(PPAR)gamma expression and its binding to target DNA sequence. Among the various upstream regulators of PPARgamma, the expression of Kruppel-like factor(KLF)2, an anti-adipogenic factor, was significantly upregulated following platycodin D treatment. When the upregulation of KLF2 was inhibited by KLF2 siRNA, the expression and binding of PPARgamma to its target sequence were significantly recovered under these conditions. The results of this study suggested that anti-adipogenic effect of platycodin D involves the upregulation of KLF2 and subsequent downregulation of PPARgamma.