RESUMO
Objective To investigate the inhibitory effect of reiniosidc C (RC) on asymmetric dimethylarginine (ADMA)-induced soluble interacellular adhesion molecule-1 (slCAM-1) expression and its mechanisms. Methods Human umbical vein endothelial cells (HUVEC 12) were cultured.The level of slCAM-1 in the conditioned medium was determined by ELISA. Changes in intracellular reactive oxygen species (ROS) levels were determined by measuring the oxidative conversion of cell permeable 2', 7'-dichlorofluorescein diacetate (DCFH-DA) to fluorescent dichlorofluorescein (DCF) in fluorospectro- photometer, and the nuclear factor-κB (NF-κB) DNA-binding activity was determined by electrophoretic mobility shift assays (EMSA). Results sICAM 1 expressions [(138.02±16.40), (194.52±11.14), (274.28±13.11)ng/L]and the generation of ROS[(75.64±5.22),(100.18±11.15),(107.23±13.45)units] in HUVEC-12 were time dependently increased by ADMA (30 μmol/L). Furthermore, thc generation of ROS [(85.33±8.68), (70.69±7.65),(59.12±4.15)units], activation of NF-κB activity and expression of sICAM-1 [(336.58±23.32),(203.27±25.18) ,(174.13±14.53)ng/L] induced by ADMA were inhibited by reinioside C (1,3,10μmol/L) in a dose-dependent manner. This effect was found to be the same by L-arginine (0.5 mmol/L) as NOS substrate and by pyrrolidine dithiocarbamate (PDTC) (10 μmol/L)as inhibitor of NF-κB.Conclusions Reinioside C attenuates the increase of sICAM-1 induced by exogenous ADMA