摘要
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。
Objective. To discuss the regulation effect of berberine on PI3K, AKT1 and GLUT1 signal pathway in HepG2 insulin resistant cells. Methods： Detected inhibition rate of different concentrations of berberine, and established insulin resistance cell model. Divided study object into five groups, including blank group, model group, metformin group, high dose of berberine group, low dose of berberine group which were given corresponding medicine. Detected expression of glucose transporter 1 （GLUT1）, phosphatidylinositol 3-kinase （PI3K）, Protein kinase B1 （AKT1） with 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 protein and GLUT1 protein in the model group was significantly lower, the expression of AKT1 protein was significantly increased（P 〈 0.05）. Compared with the model group, the expression of PI3K protein and GLUT1 protein in metformin group, high dose of berberine group and low dose of berberine group was significantly increased, the expression of AKT1 protein was significantly reduced（P〈 0.05）. Conclusion： Berberine has the effect of improving insulin resistance of cells, and its molecular mechanism may be improving insulin resistance condition by regulating the expression of transcription factor protein in PI3K, AKT1 and GLUT1 signal pathway.
出处
《新中医》
CAS
2017年第8期1-4,共4页
New Chinese Medicine
