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目的研究附子多糖对胰岛素抵抗脂肪细胞模型葡萄糖转运4(GLUT4)蛋白表达和转位的影响。方法将3T3-L1前脂肪细胞诱导分化为成熟的脂肪细胞,用高糖和高胰岛素联合诱导培养脂肪细胞,造成胰岛素抵抗脂肪细胞模型,实验设对照(CON)组、模型(MOD)组、附子多糖(FPS)组、罗格列酮(ROS)组,干预培养24 h,收集细胞,提取全细胞蛋白及细胞外膜蛋白,SDS-聚丙稀酰胺凝胶电泳后,通过Western blot方法检测各组全细胞蛋白及细胞外膜蛋白中GLUT4的含量。结果各组对GLUT4表达差异无统计学意义(P>0.05)。模型组转位显著降低,仅为正常脂肪细胞的30.4%,以模型组转位量为基值,各组分别与之相比计算GLUT4蛋白的相对定量,附子多糖组、罗格列酮组分别使GLUT4蛋白转位增加164%、301%,与模型组比较差异有统计学意义(P<0.01),附子多糖组显著低于罗格列酮组(P<0.01)。结论附子多糖对胰岛素抵抗脂肪细胞模型全细胞GLUT4蛋白表达无影响,但可促进其转位,其促进胰岛素抵抗脂肪细胞对葡萄糖的摄取可能与这一机理有关。
Objective To study the effect of aconite polysaccharide on glucose transport 4 (GLUT4) protein expression and translocation in insulin resistance adipocyte model. Methods 3T3-L1 preadipocytes were induced to differentiate into mature adipocytes. Adipocytes were cultured with high glucose and insulin to induce insulin-resistant adipocytes. CON group, model group, Polysaccharide (FPS) group and rosiglitazone (ROS) group. The cells were harvested for 24 h. The whole cell protein and extracellular membrane protein were collected. After SDS-polyacrylamide gel electrophoresis, the cells were detected by Western blot GLUT4 content in whole cell proteins and extracellular membrane proteins. Results The expression of GLUT4 in each group had no significant difference (P> 0.05). Translocation of model group was significantly reduced, only 30.4% of normal adipocytes, the model group translocation as the base, each group were compared with the relative quantification of GLUT4 protein, monkshood polysaccharide group, rosiglitazone group GLUT4 protein translocation increased 164%, 301%, compared with the model group, the difference was statistically significant (P <0.01), monkshood polysaccharide group was significantly lower than the rosiglitazone group (P <0.01). Conclusion The aconite polysaccharide has no effect on GLUT4 protein expression in whole cell of insulin resistance adipocyte model, but it can promote its translocation, which may be related to the mechanism of glucose uptake by insulin resistance adipocytes.