Inhibitory effects of rosiglitazone on activation of NF-κB and expression of ICAM-1 induced by high glucose in rat mesangial cells

Objective To investigate the role of rosiglitazone in high glucose(HG)-induced intercellular adhesion molecule-1(ICAM-1) expression of rat mesangial cells.Methods The rat mesangial cells(MCs) were cultured in the medium with normal glucose(5.6 mmol/L,NG),high glucose(25 mmol/L,HG),HG+5 μmol/L rosiglitazone,HG+20 μmol/L rosiglitazone and HG+PDTC(αNF-κB inhibitor).ICAM-1 mRNA expression was measured by semi-quantitative RT-PCR assay.Activation of nuclear factor-κB(NF-κB) of rat mesangial cells was measured by electrophoretic mobility shift assay(EMSA).The levels of ICAM-1 in the supernatants were determined by enzyme-linked immunosorbant assay(ELISA.) Results RT-PCR results showed that high-glucose increased the ratio of PCR products of ICAM-1 over GAPDH to 2.9-fold,which was prevented by rosiglitazone(5 and 20 μmol/L) pre-treatment.The NF-κB binding activity was 2.5-fold higher in MCs exposed to HG as compared with NG(P0.01).When the MCs were cultured in the presence of rosiglitazone(20 μmol/L) for 1 h,there was a highly significant reduction in NFκB binding activity(0.8±0.2 vs 2.5±0.3,P0.01).Conclusions Rosiglitazone may inhibit high glucose-induced NF-κB activation and ICAM-1 expression in mesangial cells.These findings may provide an experimental evidence for further evaluating the possibly protective effect of rosiglitazone against diabetic nephropathy.