Icariin regulates PRMT/ADMA/DDAH pathway to improve endothelial function

BackgroundOxidative stress may affect PRMT/ADMA/DDAH (protein arginine methyltransferases/asymmetric dimethylarginine/dimethylarginine dimethylaminohydrolase) pathway to impair endothelial dysfunction. The present study was carried out to test the effect of icariin on endothelial function and the mechanisms responsible for this.MethodsEighty mice at 12 weeks of age were separated randomly into four groups (n = 20): C57BL/6J control, untreated apolipoprotein E-deficient (ApoE−/−), two groups of icariin-treated (10 or 30 mg/kg body wt/day, intragastrically) ApoE−/−. Primary human umbilical vein endothelial cells (HUVECs) were randomly divided into 7 groups: control group, vehicle of icariin (10 μmol/L) group, icariin (10 μmol/L) group, lysophosphatidylcholine (LPC) (10 μg/mL) group, LPC plus icariin (1 μmol/L) group, LPC plus icariin (3 μmol/L) group, and LPC plus icariin (10 μmol/L) group.ResultsIn ApoE−/− mice and primary HUVECs, icariin treatment decreased reactive oxygen species production, PRMT I expression, ADMA level, half-maximum effective concentration of ApoE−/− mice aortic rings. Icariin increased DDAH II expression, DDAH activity, maximal relaxation value and endothelium-dependent vasorelaxation in aortic rings from ApoE−/− mice (p < 0.05 or p < 0.01).ConclusionsThe present results suggest that icariin regulates PRMT/ADMA/DDAH pathway to improve endothelial function.