AB184. Icariside II induces NO production in human cavernous endothelial cells via the activation of eNOS by miR-155

Objective: To investigate the status miR-155 and its targeting eNOS under the stimulation of glucose and age-BSA and to explore the effect of icariside II (ICA II) on the diabetic endothelial dysfunction of human cavernous endothelial cells (HCECs) by using the miR-155 pathway.

Methods: Purified HCECs were divided into three groups: normal group + BSA (NC group), Glucose + Age-BSA group (DM group), ICA II treatment group (DM + ICA II group). Western blot to detect the expression of eNOS and RAGE protein expression; immunofluorescence assay to detect the NO production; real time PCR to detect the expression of miR-155 and eNOS. Overexpression of miR-155 was performed in HCECs with or without ICA II interference.

Results: Under the diabetic induction, the expression of eNOS in DM group is significantly reduced compared with that in NC group and the expression of RAGE in DM group is significantly up-regulated compared with that in NC group (P<0.05), but the DM + ICA II group showed higher eNOS expression and lower RAGE expression compared with those in the DM group. MiR-155 is higher after overexpression but can be repressed by ICA II, eNOS expression was lower after overexpression but was increased by ICA II.

Conclusions: Under the glucose and Age-BSA stimulation, ICA II may induce NO production in HCECs via the activation of eNOS by miR-155 so as to restore the HCECs functions.

Keywords: Icariside II (ICA II); microRNA; diabetes mellitus