[C21 inhibits cytokine secretion in rat renal tubular epithelial cells stimulated by advanced glycation end products].

Abstract

Objective To investigate the effect and mechanism of compound 21(C21), an agonist of angiotensin II-2 receptor (AT2R) on the cytokine levels of NRK-52E cells stimulated by advanced glycation end products bovine serum albumin (AGE-BSA). Methods NRK-52E cells were divided into control and (25, 50, 100, 200)mg/L AGE-BSA groups and cultured for 48 hours. The mRNA and protein expression levels of leukin-6 (IL-6) and tumor necrosis factor α (TNF-α) were detected by real-time quantitative PCR and ELISA. The NRK-52E cells stimulated by AGE-BSA(25 mg/L) for 48 hours were then treated with (0.01, 0.05, 0.1)mmol/L C21 for 24 hours. The mRNA and protein expression levels of protein kinase C (PKC), nuclear factor κB p65 (NF-κB p65) and transforming growth factor β1 (TGF-β1) were detected by qRT-PCR and Western blot analysis. Results The mRNA expression levels of IL-6 and TNF-α significantly increased in NRK-52E cells stimulated by AGE-BSA at different doses, with the greatest increase in the 25 mg/L AGE-BSA group. The mRNA and protein expression levels of PKC, NF-κB p65 and TGF-β1 in AGE-BSA-induced NRK-52E cells significantly decreased by (0.01, 0.05, 0.1)mmol/L C21. Conclusion AGE-BSA promotes the expression of IL-6, TNF-α, PKC, NF-κB p65 and TGF-β1 in NRK-52E cells, while C21 inhibits the effect of AGE-BSA on NRK-52E cells.