关键词: 矢车菊素-3-O-β-D-葡萄糖苷, 核受体, 萤光素酶报告基因, 转录活性

Abstract: The effects of anthocyanin [cyanidin-3-O-β-D-glucoside (C3G)] and its aglycone [cyanidin] on transcriptional activity of nuclear receptors closely related to metabolic syndrome were investigated. Human liver LO2 cells were transfected with several plasmids including retinoid X receptor (RXR), pregnane X receptor (PXR), estrogen receptor (ER), farnesol X receptor (FXR), liver X receptors (LXRα and LXRβ), and peroxisome proliferator activated receptors (PPARα, PPARγ and PPARδ), respectively. Plasmids with the nuclear receptor element luciferase gene, and green fluorescent protein were constructed as nuclear receptor reporter models. The transfected cells were cultured with media containing cyanidin or C3G at the concentrations of 1, 10 μmol/L and 100 μmol/L, respectively for 24 h. The results indicated that RXR was inhibited by cyaniding at all concentrations tested, and only PXR model was slightly stimulated by cyanidin at the concentration of 100 μmol/L (1.42 ± 0.19 fold, P <0.05 compared with 0.1% DMSO as the control). However, other nuclear receptors including PXR, ER, LXRα, LXRβ, PPARγ and PPARδ could be significantly stimulated by C3G (P <0.05), and the transcriptional activity of PXR, LXRα, LXRβ and PPARγ could be increased by over 50% when compared to 0.1% DMSO. Therefore, the mechanism of anthocyanidin improving metabolic syndrome was likely to be correlated with its augmentative effect on transcriptional activity of nuclear receptors, and it could be concluded that C3G was generally more effective than its aglycone cyanidin.

Key words: cyanidin-3-O-β-D-glucoside, nuclear receptor, luciferase reporter gene, transcriptional activity