目的评价玫瑰花提取物的体外降糖活性,研究玫瑰花多酚作用的胰岛素信号通路并阐明其降糖作用机制。方法采用脂质体介导的质粒转染法构建蛋白酪氨酸磷酸酶-1B(PTP1B)蛋白过表达的CHO-K1细胞模型,通过蛋白印迹分析法(Western blotting)研究玫瑰花多酚对细胞内信号分子蛋白表达量的影响。结果体外玫瑰花提取物抑制PTP1B酶活性,半数抑制浓度(IC50)为62.31 ng·m L-1。玫瑰花提取物可提高细胞葡萄糖消耗,与阳性对照药作用相当;在细胞内可明显提高磷酸化的胰岛素受体底物1(IRS-1)、磷脂酰肌醇依赖性激酶1(PDK1)、蛋白激酶B(AKT)以及糖原合成激酶3β(GSK-3β)蛋白表达量。结论玫瑰花提取物对PTP1B有良好的抑制活性,可促进葡萄糖消耗,具有潜在降糖活性;玫瑰花提取物通过增加IRS-1、下游信号分子PDK1、AKT以及GSK-3β蛋白的磷酸化水平来激活PI3K/AKT胰岛素信号通路,从而促进胰岛素信号传导和糖原合成,达到降低血糖的效果。 Objective To evaluate the hypoglycemic activity of rose extract in vitro and to study the insulin signaling pathway of rose polyphenols and to elucidate the hypoglycemic mechanism. Methods CHO-K1 cell model of overexpression of protein tyrosine phosphatase-1B (PTP1B) was constructed by lipofectamine mediated transfection. Western blotting was used to study the effect of rosette polyphenols on cell proliferation Effect of internal signal protein expression. Results In vitro rose extract inhibited the activity of PTP1B, with a half-maximal inhibitory concentration (IC50) of 62.31 ng · m L-1. Rose extract can increase cell glucose consumption, which is equivalent to that of the positive control drug; phosphorylation of insulin receptor substrate 1 (IRS-1), phosphatidylinositol-dependent kinase 1 (PDK1) Protein kinase B (AKT) and glycogen synthesis kinase 3β (GSK-3β) protein expression. Conclusion Rose extract has good inhibitory activity on PTP1B, which can promote glucose consumption and has potential hypoglycemic activity. Rose extract can increase phosphoprotein levels of IRS-1, downstream signaling molecules PDK1, AKT and GSK-3β Activate the PI3K / AKT insulin signaling pathway, thereby promoting insulin signaling and glycogen synthesis, to reduce blood sugar effect.