Effect of puerarin on insulin resistance in 3T3-L1 adipocytes and its mechanism
Objective:To investigate the effect of puerarin on insulin resistance(IR)in 3T3-L1 adipocytes and its possible mechanism.Methods:3T3-L1 adipocytes were divided into 7 groups,namely control group,3 μmol/L puerarin group,10 μmol/L puerarin group,30 μmol/L puerarin group,100 μmol/L puerarin group,300 μmol/L puerarin group,and positive control group(rosiglitazone 10 μmol/L group,RGZ group),with 6 Wells in each group.Cell proliferation was detected by MTT assay,and adipocyte differentiation was detected by oil red O staining.The IR model of 3T3-L1 adipocytes was established by dexamethasone induction,and the glucose utili-zation was measured after different concentrations of puerarin treatment.Cells were transfected to over-express TLR2(Pue+oe-TLR2 group).The levels of TLR2 proteins were determined by western blotting and the levels of interferon-γ(IFN-γ)were determined by enzyme-linked immunosorbent assay(ELISA).Results:Compared with the control group,there was no significant change in the proliferation of 3T3-L1 adipocytes in the puerarin treat-ment groups(P＞0.05).Compared with the control group,the differentiation of 3T3-L1 adipocytes was signifi-cantly promoted in the puerarin treatment groups(P＜0.05).Compared with the control group,the glucose con-sumption of IR 3T3-L1 adipocytes was significantly increased in the puerarin treatment groups(P＜0.05).The ex-pression of TLR2 and the secretion of IFN-γ in IR 3T3-L1 adipocytes were decreased,and the levels of GLUT4 and PPARγ were increased in the puerarin treatment groups(P＜0.05).The relative expression of TLR2 and the secretion of IFN-γ in the Pue+oe-TLR2 group were significantly higher than those in the Pue+oe-NC group,and the relative expression of PPARγ and GLUT4 was significantly lower than that in the Pue+oe-NC group(P＜0.01).Conclusion:Pue-rarin can increase the glucose consumption of IR3T3-L1 adipocytes and alleviate IR.Its mechanism may be related to the inhibition of TLR2 expression and the reduction of IFN-γ secretion.
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