The objective of this study was to investigate the effects of resistin on insulin signaling in human umbilical vein endothelial cells(HUVECs).HUVECs were incubated with recombinant human resistin(0–100 ng/mL)for 24 h...The objective of this study was to investigate the effects of resistin on insulin signaling in human umbilical vein endothelial cells(HUVECs).HUVECs were incubated with recombinant human resistin(0–100 ng/mL)for 24 h.Akt and endothelial nitric oxide synthase(eNOS)phosphorylation levels of endothelial cells under basal or insulin stimulated conditions were measured by Western blot.Nitric oxide(NO)production of HUVECs was also detected.The results showed that resistin could significantly inhibit Akt and eNOS phos-phorylation and NO production in endothelial cells under insulin stimulated conditions(P<0.05 vs control).But under basal conditions,treatment with resistin could result in a decrease in eNOS phosphorylation(P<0.05 vs control)but had no effect on NO production and Akt phosphorylation levels.Thesefindings suggested that resistin exerted an inhibitory effect on NO production by inhibiting insulin signaling and eNOS phosphorylation in endothelial cells.展开更多
基金supported by the National Natural Science Foundation of China(Grant No.30570886).
文摘The objective of this study was to investigate the effects of resistin on insulin signaling in human umbilical vein endothelial cells(HUVECs).HUVECs were incubated with recombinant human resistin(0–100 ng/mL)for 24 h.Akt and endothelial nitric oxide synthase(eNOS)phosphorylation levels of endothelial cells under basal or insulin stimulated conditions were measured by Western blot.Nitric oxide(NO)production of HUVECs was also detected.The results showed that resistin could significantly inhibit Akt and eNOS phos-phorylation and NO production in endothelial cells under insulin stimulated conditions(P<0.05 vs control).But under basal conditions,treatment with resistin could result in a decrease in eNOS phosphorylation(P<0.05 vs control)but had no effect on NO production and Akt phosphorylation levels.Thesefindings suggested that resistin exerted an inhibitory effect on NO production by inhibiting insulin signaling and eNOS phosphorylation in endothelial cells.
