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一种来自云芝的多糖通过Akt-GSK-3信号通路缓解HepG2细胞的胰岛素抵抗。

A polysaccharide from Grifola frondosa relieves insulin resistance of HepG2 cell by Akt-GSK-3 pathway.

作者信息

Ma Xiaolei, Zhou Fuchuan, Chen Yuanyuan, Zhang Yuanyuan, Hou Lihua, Cao Xiaohong, Wang Chunling

机构信息

Key Laboratory of Food Nutrition and Safety, Ministry of Education, College of Food Engineering and Biotechnology, Tianjin University of Science & Technology, Tianjin, 300457, People's Republic of China.

出版信息

Glycoconj J. 2014 Jul;31(5):355-63. doi: 10.1007/s10719-014-9526-x. Epub 2014 Jun 8.

DOI:10.1007/s10719-014-9526-x
PMID:24908430
Abstract

Grifola frondosa is an important fungal research resource. However, there was little report about hyperglycemic activity of Grifola frondosa polysaccharide on insulin resistance in vitro. In this study, the hypoglycemic activity of a polysaccharide obtained from Grifola frondosa (GFP) on HepG2 cell and hpyerglycemic mechanism were investigated. The purity of the isolated polysaccharides was examined by HPLC. In this research, it was found that GFP enhanced the absorption of glucose of HepG2 cells in a dose dependent manner at 24 h of 30 ugmL⁻¹. GC-MS and FT-IR spectroscopy analysis results showed that glucose and galactose were the dominant monosaccharides in GFP and the major component of GFP was β-pyranoside. Western-blotting results showed that the HepG2 cell model treated with GFP activated the insulin receptor protein (IRS) in the cell membrane and increased phosphorylated-AktSer473 expression, which had an inhibition of glycogen synthase kinase (GSK-3). The down-regulation of GSK-3 stimulated synthesis of intracellular glycogen. The results above suggested that the GFP increased the metabolism of glucose and stimulated synthesis of intracellular glycogen through the Akt/GSK-3 pathway.

摘要

灰树花是一种重要的真菌研究资源。然而,关于灰树花多糖对胰岛素抵抗的体外降血糖活性的报道较少。在本研究中,研究了从灰树花中获得的一种多糖(GFP)对HepG2细胞的降血糖活性及其降血糖机制。通过高效液相色谱法检测分离多糖的纯度。在本研究中,发现GFP在30μgmL⁻¹浓度下作用24小时,以剂量依赖的方式增强了HepG2细胞对葡萄糖的摄取。气相色谱-质谱联用(GC-MS)和傅里叶变换红外光谱(FT-IR)分析结果表明,葡萄糖和半乳糖是GFP中的主要单糖,GFP的主要成分是β-吡喃糖苷。蛋白质免疫印迹(Western-blotting)结果显示,用GFP处理的HepG2细胞模型激活了细胞膜中的胰岛素受体蛋白(IRS),并增加了磷酸化AktSer473的表达,这对糖原合酶激酶(GSK-3)有抑制作用。GSK-3的下调刺激了细胞内糖原的合成。上述结果表明,GFP通过Akt/GSK-3途径增加了葡萄糖的代谢并刺激了细胞内糖原的合成。

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