Androgen Replacement Therapy Improves Erectile Dysfunction In Castrated Rats Through Inhibition Of Endothelial Dysfunction And Corporal Fibrosis

To investigate the detailed mechanism that androgen replacement therapy improves erectile dysfunction in castrated rats through inhibition of endothelial dysfunction and corporal fibrosis. We divided 40, 8-week-old healthy male rats randomly into four groups: normal control group (Control); Castration group (Castration); Other 20 rats were castrated followed by testosterone (T) undecanoate (orally) each day, and they were divided into: Castration + 10mg/kg T group (Castration + 10T) and Castration + 20 mg/kg T group (Castration + 20T). After 8 weeks of treatment, serum levels of T and erectile function were assessed. Western blotting, Immunofluorescence and immunohistochemistry were performed to detect levels of target proteins. Serum levels of testosterone and erectile function in Castration group were significantly lower than those in other groups; Expression of von Willebrand factor (vWF), CD31 and eNOS in Castration group was lower than that in other groups; Expression of α-smooth muscle actin (α-SMA) in Castration group was lower than that in other groups, while transforming growth factor (TGF-β) was higher; Expression of androgen receptor/vascular endothelial growth factor/cyclinA (AR/VEGF/cyclinA) in Castration group was lower than that in other groups; Expression of sphingosine-1-phosphate receptor 2 (S1P2)/ROCK/LIMK2/Cofilin was higher in Castration group than that in other groups.