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日本蓟黄酮可促进 3T3-L1 细胞中的脂肪细胞分化和葡萄糖摄取。

Cirsium japonicum flavones enhance adipocyte differentiation and glucose uptake in 3T3-L1 cells.

机构信息

College of Life and Environmental Science, Wenzhou University, China.

出版信息

Biol Pharm Bull. 2012;35(6):855-60. doi: 10.1248/bpb.35.855.

Abstract

Cirsium japonicum flavones have been demonstrated to possess anti-diabetic effects in diabetic rats, but the functional mechanism remains unknown. The nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ) plays an important role in glucose and lipid homeostasis. In this study, we report the effects of Cirsium japonicum flavones (pectolinarin and 5,7-dihydroxy-6,4-dimethoxy flavone) on PPARγ activation, adipocyte differentiation, and glucose uptake in 3T3-L1 cells. Reporter gene assays and Oil Red O staining showed that Cirsium japonicum flavones induced PPARγ activation and enhanced adipocyte differentiation of 3T3-L1 cells in a dose-dependent manner. In addition, Cirsium japonicum flavones increased the expression of PPARγ target genes, such as adiponectin and glucose transporter 4 (GLUT4), and enhanced the translocation of intracellular GLUT4 to the plasma membrane. In mature 3T3-L1 adipocytes, Cirsium japonicum flavones significantly enhanced the basal and insulin-stimulated glucose uptake. The flavones-induced effects in 3T3-L1 cells were abolished by the PPARγ antagonist, GW9662, and by the phosphatidylinositol 3-kinase (PI3K) inhibitor, wortmannin. This study suggests that Cirsium japonicum flavones promote adipocyte differentiation and glucose uptake by inducing PPARγ activation and then modulating the insulin signaling pathway in some way, which could benefit diabetes patients.

摘要

刺儿菜黄酮已被证明在糖尿病大鼠中具有抗糖尿病作用,但功能机制尚不清楚。核受体过氧化物酶体增殖物激活受体γ(PPARγ)在葡萄糖和脂质稳态中发挥重要作用。在这项研究中,我们报告了刺儿菜黄酮(佩可啉和 5,7-二羟基-6,4-二甲氧基黄酮)对 3T3-L1 细胞中 PPARγ 激活、脂肪细胞分化和葡萄糖摄取的影响。报告基因检测和油红 O 染色显示,刺儿菜黄酮以剂量依赖的方式诱导 PPARγ 激活并增强 3T3-L1 细胞的脂肪细胞分化。此外,刺儿菜黄酮增加了 PPARγ 靶基因的表达,如脂联素和葡萄糖转运蛋白 4(GLUT4),并增强了细胞内 GLUT4 向质膜的易位。在成熟的 3T3-L1 脂肪细胞中,刺儿菜黄酮显著增强了基础和胰岛素刺激的葡萄糖摄取。PPARγ 拮抗剂 GW9662 和磷脂酰肌醇 3-激酶(PI3K)抑制剂wortmannin 可消除黄酮类化合物对 3T3-L1 细胞的影响。这项研究表明,刺儿菜黄酮通过诱导 PPARγ 激活,然后以某种方式调节胰岛素信号通路,促进脂肪细胞分化和葡萄糖摄取,这可能使糖尿病患者受益。

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