Effects of Inhibiting Nuclear Factor-kappa B Activity on Expression of AngiotensinII Type-1 Receptor in Glomerular Mesangial Cells of Sprague Dawley Rats

【Objective】 To study the effects of inhibiting nuclear factor-kappa B (NF-κB) activity on the expression of angiotensinⅡtype-1 receptor (AT1R) mRNA in mesangial cells (MC) of Sprague Dawley (SD) rats. 【Methods】 MCs of SD rats were isolated and divided into three groups as fallows: cultured with normal glucose (5.6 mmol / L D-glucose), high glucose (25 mmol / L D-glucose) and pyrrolidinedithiocarbamate (PDTC) + high glucose. The NF-B activity was measured by electrophoretic mobility shift assay. The expression of angiotensinⅡtype-1 receptor was measured by RT-PCR for mRNA and by Western blot for protein. The angiotensinⅡin supernatant was measured by radioimmunoassay (RIA). 【Results】 The NF-κB activity in the MCs cultured with high glucose (20 ± 7) was significantly higher than those in the MCs cultured with normal glucose (8 ± 4, P 0.01) and PDTC + high glucose (8 ± 3, P 0.01), and had no significant difference between normal glucose and PDTC + high glucose. There were no significant differences of AT1R mRNA levels among the MCs cultured with high glucose (0.60 ± 0.26), normal glucose (0.50 ± 0.22) and PDTC + high glucose (0.45 ± 0.23), and also no significant differences of AT1R protein levels among the MCs cultured with high glucose (0.54 ± 0.22), normal glucose (0.37 ± 0.14) and PDTC + high glucose (0.40 ± 0.13). The angiotensinⅡlevel of supernatant in the MCs cultured with high glucose (9.8 ± 2.1) was significantly higher than that in the MCs cultured with normal glucose (7.5±1.5, P 0.05), and had no significant difference between PDTC+ high glucose (7.8 ± 1.7, P 0.05) and normal glucose. 【Conclusion】 High glucose can increase the NF-κB activity of MCs and the angiotensinⅡlevel of supernatant, but can not change the expression of AT1R mRNA and protein of MCs. Inhibiting NF-κB activity may decrease the angiotensinⅡlevel of supernatant but have no effect on the expression of AT1R mRNA and protein of MCs.