Department of Microbiology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
Phytother Res. 2010 Jun;24 Suppl 2:S161-7. doi: 10.1002/ptr.3054.
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.
在这项研究中，发现远志酸 D 能够抑制 3T3-L1 细胞内的甘油三酯积累，其 IC（50）为 7.1μM。用远志酸 D 处理后，参与脂代谢的基因如脂肪酸结合蛋白 4 和脂蛋白脂肪酶的表达水平显著下调。远志酸 D 处理还导致过氧化物酶体增殖物激活受体（PPAR）γ的表达及其与靶 DNA 序列的结合减少。在 PPARγ的各种上游调节剂中，反脂肪生成因子 KLF2 的表达在远志酸 D 处理后显著上调。当通过 KLF2 siRNA 抑制 KLF2 的上调时，在这些条件下，PPARγ的表达及其与靶序列的结合明显恢复。本研究结果表明，远志酸 D 的抗脂肪生成作用涉及 KLF2 的上调和随后的 PPARγ下调。
