| Purpose:To establishment3T3-L1adipocytes cells3-Deoxyglucosone (3-DG)-induced insulin resistance (IR) cell model, and applied to the intervention studies on Apigenin and other drugs. Methods:(1) In vitro isolation of rat primary adipocytes were randomly divided into3-DG and control groups. The role of different concentrations of3-DG48h, using glucose oxidase peroxidase method (GOD-POD method) to determine the cell glucose consumption inhibition in a dose-dependent manner.(2) In vitro cultured3T3-L1fat cells, with different concentrations of3-DG role to the glucose oxidase-peroxidase enzymatic (GOD-POD method) measured residual content of glucose in the culture solution, to observe the3-DG impact of sugar consumption of fat cells, observed by western blotting protein-mediated sugar transporter3-DG3T3-L1adipocyte glucose transporter (GLUT4), insulin signaling pathway PI-3K/AKT ways impact, full identification of the IR model.(3)3-DG role in3T3-L1adipocytes cells, the culture medium were added to apigenin, narinenin, puerarin cells was measured glucose consumption, and explore the apigenin improved3-DG damage fat cells insulin possible mechanisms of resistance. Results:(1)3-DG primary adipocytes glucose consumption decreased.(2)3-DG glucose consumption in3T3-L1adipocytes cells reduced;3-DG decreased expression of the3T3-L1adipocytes the cell GLUT4protein;3-DG of Akt in3T3-L1adipocytes cells, the p85protein decreased expression.(3) Different drugs, and3-DG at the same time acts on3T3-L1fat cells, can improve the effect of3T3-L1adipocyte glucose consumption3-DG. Conclusion:3-DG3T3-L1adipocytes cells can induce insulin resistance; this cell model is simple and reliable. Apigenin, Naringenin, Puerarin obviously improve the3-DG inducing3T3-L1preadipocytes insulin resistance effect. |