Icariside II prevents high-glucose-induced injury on human cavernous endothelial cells through Akt-eNOS signaling pathway.

Dysfunction of human cavernous endothelial cells (HCECs) is a common pathological alteration caused by elevated high blood glucose levels associated with diabetes. To explore the protective effects of Icariside II (ICA II) on human cavernous endothelial cells, HCECs were isolated from non-diabetic human donors, cultured under high glucose (HG) conditions and treated with ICA II. The cell apoptosis and proliferation, expression of Ki67 and Erk1/2, antioxidant capacity, and expression of Akt and eNOS were examined. Changes in cell apoptosis and proliferation indicated that HG treatment inhibited HCEC proliferation with lower percentage of Ki67-positive cells and lower expression and phosphorylation of Erk1/2. Furthermore, the total antioxidant capacity (T-AOC) of HCECs was reduced under HG conditions. In line with these findings, both expression and phosphorylation of Akt as well as eNOS was down regulated after HG treatment. The reduction in proliferative capacity, p-Erk1/2, p-Akt, and p-eNOS were partially prevented by ICA II in a concentration-dependent manner. The protective effects of ICA II rescued HCEC from injury and dysfunction induced by HG in vitro. ICA II may be a candidate for prevention of the development of diabetic erectile dysfunction.