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目的 :探讨小檗碱对Hep G2胰岛素抵抗细胞PI3K/AKT1/GLUT1信号通路的调控作用。方法 :MTT法检测小檗碱不同浓度对细胞生长的抑制率;建立胰岛素抵抗细胞模型,实验分为5组,分别为空白组、模型组、二甲双胍组、小檗碱高剂量组、小檗碱低剂量组,给予相应的药物后,Western Blot检测葡萄糖转运蛋白1(GLUT1)、磷脂酰肌醇激酶(PI3K)、蛋白激酶B1(AKT1)的表达。结果:与空白组比较,模型组细胞培养基中的葡萄糖含量显著升高,差异有统计学意义(P<0.05),说明胰岛素抵抗细胞模型建立成功。与空白组比较,模型组PI3K蛋白、GLUT1蛋白表达显著降低,AKT1蛋白表达显著升高,差异均有统计学意义(P<0.05)。与模型组比较,二甲双胍组、小檗碱高剂量组、小檗碱低剂量组PI3K蛋白、GLUT1蛋白表达显著升高,AKT1蛋白表达显著降低,差异均有统计学意义(P<0.05)。结论:小檗碱具有改善细胞胰岛素抵抗的作用,其分子机制可能通过调控PI3K/AKT1/GLUT1信号通路中转录因子蛋白的表达,从而改善细胞胰岛素抵抗状态。
AIM: To investigate the regulatory effect of berberine on PI3K / AKT1 / GLUT1 signaling pathway in Hep G2 insulin resistance cells. Methods: MTT method was used to detect the inhibitory rate of berberine at different concentrations on cell growth. The model of insulin resistance was established. The experiment was divided into 5 groups: blank group, model group, metformin group, berberine high dose group, berberine Low dose group. After the corresponding drugs were given, the expression of glucose transporter 1 (GLUT1), phosphatidylinositol kinase (PI3K) and protein kinase B1 (AKT1) were detected by Western Blot. Results: Compared with the blank group, the glucose content in the cell culture medium of the model group was significantly increased (P <0.05), indicating that the insulin resistance cell model was established successfully. Compared with the blank group, the expression of PI3K, GLUT1 and AKT1 in model group were significantly decreased (P <0.05). Compared with the model group, the expression of PI3K protein and GLUT1 protein in the metformin group, berberine high-dose group and berberine low-dose group were significantly increased, AKT1 protein expression was significantly decreased (P <0.05). CONCLUSION: Berberine can improve the insulin resistance of cells, and its molecular mechanism may improve the insulin resistance by regulating the expression of transcription factor PI3K / AKT1 / GLUT1 signaling pathway.