Nishina Atsuyoshi, Itagaki Masaya, Suzuki Yuusuke, Koketsu Mamoru, Ninomiya Masayuki, Sato Daisuke, Suzuki Takashi, Hayakawa Satoshi, Kuroda Makoto, Kimura Hirokazu
College of Science and Technology, Nihon University, 1-5-1 Kandasurugadai, Chiyoda, Tokyo 101-0062, Japan.
Department of Chemistry and Biomolecular Science, Faculty of Engineering, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan.
Molecules. 2017 Apr 22;22(4):671. doi: 10.3390/molecules22040671.
(Makino) Koidz. is a local product from the area in and around Yonezawa City in Yamagata Prefecture, Japan. It has been used as a medicinal plant for a long time. We isolated and identified four types of flavonoid glycosides [astragalin (), isoquercetin (), rhamnocitrin 3--glucoside (), and nicotiflorin ()], a triterpene [methyl hederagenin ()], and three types of triterpene glycosides [δ-hederin (), echinocystic acid 3--arabinoside (), and cauloside B ()] from the methanol extract of , which regulates lipid accumulation in 3T3-L1 preadipocytes. Among the compounds isolated, and up- and down-regulated lipid accumulation and insulin induced adipocyte differentiation in 3T3-L1 preadipocytes. Compound induced up-regulation of lipid accumulation and decreased adipocyte size, while down-regulated lipid accumulations without decreasing cell size. Additionally, increased adipogenic proteins [peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), and fatty-acid-binding protein 4 (FABP4)]. In contrast, decreased the levels of all adipogenic proteins and glucose transporter type 4 (GLUT4), but increased adiponectin.
（牧野）小出（Koidz.）是日本山形县米泽市及其周边地区的本土产物。长期以来它一直被用作药用植物。我们从其甲醇提取物中分离并鉴定出四种黄酮类糖苷[紫云英苷（astragalin）、异槲皮苷（isoquercetin）、鼠李柠檬素3 - O - 葡萄糖苷（rhamnocitrin 3 - O - glucoside）和烟花苷（nicotiflorin）]、一种三萜[甲基常春藤皂苷元（methyl hederagenin）]以及三种三萜糖苷[δ - 常春藤皂苷（δ - hederin）、刺囊酸3 - O - 阿拉伯糖苷（echinocystic acid 3 - O - arabinoside）和茎糖苷B（cauloside B）]，该提取物可调节3T3 - L1前脂肪细胞中的脂质积累。在分离出的化合物中，[此处原文似乎有缺失化合物名称]和[此处原文似乎有缺失化合物名称]分别上调和下调了3T3 - L1前脂肪细胞中的脂质积累以及胰岛素诱导的脂肪细胞分化。化合物[此处原文似乎有缺失化合物名称]诱导脂质积累上调并减小脂肪细胞大小，而[此处原文似乎有缺失化合物名称]下调脂质积累但不减小细胞大小。此外，[此处原文似乎有缺失化合物名称]增加了脂肪生成蛋白[过氧化物酶体增殖物激活受体γ（PPARγ）、CCAAT/增强子结合蛋白α（C/EBPα）和脂肪酸结合蛋白4（FABP4）]。相反，[此处原文似乎有缺失化合物名称]降低了所有脂肪生成蛋白和4型葡萄糖转运蛋白（GLUT4）的水平，但增加了脂联素。
