摘要
目的:探讨桑叶生物碱、黄酮及多糖对Hep G2细胞胰岛素抵抗的改善及其作用机制。方法:采用高糖高胰岛素培养基诱导Hep G2细胞形成红外(IR)模型,葡萄糖氧化酶法检测正常组、模型组、罗格列酮组、生物碱组、黄酮组及多糖组的细胞葡萄糖消耗情况,并用RT-q PCR法检测C-Jun氨基端激酶(JNK)通路相关基因的表达,观察桑叶生物碱、黄酮及多糖改善Hep G2细胞胰岛素抵抗及其作用机制。结果:高糖及高胰岛素培养基培养Hep G2细胞,使细胞葡萄糖消耗率明显下降,造成胰岛素抵抗的细胞模型,给予桑叶生物碱、黄酮及多糖干预之后,细胞葡萄糖消耗率明显上升,同时下调JNK和上调IRS-1,AKT mRNA的表达。结论:桑叶生物碱、黄酮及多糖均可增加Hep G2细胞的葡萄糖消耗量,其改善胰岛素抵抗作用可能与调节JNK信号通路有关。
Objective:To investigate the protective effect and its mechanism of different effective extracts of Mori Folium on the infrared (IR) model of HepG2 cells.Method:High glucose and insulin in HepG2 cells to form a cell model of insulin resistance,glucose oxidase detect the expression of glucose consumption,and using the real-time fluorescent quantitative polymerase chain reaction (PCR) technique to observe the expression level of C-Jun amino termind kinose (JNK) pathway related genes in different effective extracts of Mori Folium on the IR model of HepG2 cells.Result:High sugar and high insulin culture environment capable of inducing cells to produce insulin resistance.All of the groups can increase the glucose consumption (P < 0.01) and has the influence on the expression of JNK related genes.Conclusion:The alkaloids,flavonoids and polysaccharides of mulberry leves can increase the glucose consumption on the HepG2 cells,which may be related to regulating JNK signaling pathways.
出处
《中国实验方剂学杂志》
CAS
CSCD
北大核心
2015年第2期192-195,共4页
Chinese Journal of Experimental Traditional Medical Formulae
基金
广东省科技计划项目(2011A080300004)