Graduate School of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura-cho, Nagahama-shi, Shiga, 526-0829, Japan.
Graduate School of Biosphere Science, Hiroshima University, 1-7-1 Kagamiyama, Higashi-Hiroshima, 739-8521, Japan.
Mol Cell Biochem. 2018 Sep;446(1-2):35-41. doi: 10.1007/s11010-018-3270-7. Epub 2018 Jan 9.
Peroxisome proliferator-activated receptors (PPARs) are ligand-dependent transcription factors that regulate lipid and glucose metabolism. PPARα mainly affects fatty acid metabolism, and its activation lowers lipid levels. PPARγ is involved in the regulation of adipogenesis, insulin sensitivity, energy balance, and lipid biosynthesis. We have previously reported that 4',6-dimethoxyisoflavone-7-O-β-D-glucopyranoside (wistin) can activate PPARγ. The purpose of the present study is to investigate the PPARα agonist activity of wistin. Using a luciferase reporter assay system of PPARα in monkey COS7 kidney cells, we showed that wistin could activate PPARα (P < 0.01 at 10 μg/mL) in a dose-dependent manner. Moreover, the addition of wistin upregulated the expression of PPARα (P < 0.01 at 10 μg/mL) and PPARα target genes including carnitine palmitoyltransferase 1a (P < 0.05 at 10 μg/mL), acyl-CoA oxidase (P < 0.01 at 10 μg/mL), acyl-CoA synthase (P < 0.05 at 10 μg/mL), PPARγ coactivator 1α (P < 0.05 at 10 μg/mL), uncoupling protein 2 (P < 0.05 at 1 μg/mL), and uncoupling protein 3 (P < 0.05 at 10 μg/mL), which are genes involved in lipid efflux and energy expenditure, in mouse primary hepatocytes. Furthermore, wistin inhibited cellular triglyceride accumulation in hepatocytes (P < 0.05 at 10 μg/mL) in a dose-dependent manner. These results indicate that wistin could suppress lipid accumulation through PPARα activation. The action of wistin on PPARα could be of interest for the amelioration of lipid metabolic disorders. To the best of our knowledge, wistin is the first reported isoflavonoid O-glycoside with PPARα agonist activity.
过氧化物酶体增殖物激活受体 (PPARs) 是配体依赖性转录因子,可调节脂质和葡萄糖代谢。PPARα 主要影响脂肪酸代谢,其激活可降低脂质水平。PPARγ 参与调节脂肪生成、胰岛素敏感性、能量平衡和脂质生物合成。我们之前报道过 4',6-二甲氧基异黄酮-7-O-β-D-吡喃葡萄糖苷(wistin)可激活 PPARγ。本研究旨在探讨 wist in 对 PPARα 的激动剂活性。我们在猴 COS7 肾细胞中的 PPARα 荧光素酶报告基因检测系统中显示,wistin 可剂量依赖性地激活 PPARα(10μg/mL 时 P<0.01)。此外,wistin 的添加上调了 PPARα 的表达(10μg/mL 时 P<0.01)及其靶基因,包括肉碱棕榈酰基转移酶 1a(10μg/mL 时 P<0.05)、酰基辅酶 A 氧化酶(10μg/mL 时 P<0.01)、酰基辅酶 A 合成酶(10μg/mL 时 P<0.05)、PPARγ 共激活因子 1α(10μg/mL 时 P<0.05)、解偶联蛋白 2(1μg/mL 时 P<0.05)和解偶联蛋白 3(10μg/mL 时 P<0.05),这些基因参与脂质流出和能量消耗,在小鼠原代肝细胞中。此外,wistin 以剂量依赖性方式抑制肝细胞中的细胞内甘油三酯积累(10μg/mL 时 P<0.05)。这些结果表明,wistin 通过激活 PPARα 抑制脂质积累。wistin 对 PPARα 的作用可能有助于改善脂质代谢紊乱。据我们所知,wistin 是第一个报道具有 PPARα 激动剂活性的异黄酮 O-糖苷。