[A low androgen state impairs erectile function by suppressing the expression of Tie2 in rat penile cavernosa]

To investigate whether androgens regulate the expression of endothelial nitric oxide synthase (eNOS) in rat penile cavernous tissue through endothelial-rich adventitial endothelial cell kinase 2 (Tie2)/phosphokinase (AKT) and affect penile erectile function.

Eight-week-old male SD (Sprague Dawley) rats were randomly divided into 6 groups (n=6): sham group, cast group, cast+testosterone replacement group (cast+T group, subcutaneous injection of testosterone propionate 3mg/kg every other day after castration), sham+Tie2 transfection group (sham+Tie2 group, 20ul Tie2 gene lentivirus injection into penile cavernosa of rats 4 weeks after castration, titer 1×108TU/ml), cast+Tie2 group, cast+empty vector group. Five weeks after castration, the ratio of maximum penile intracavernous pressure to mean arterial pressure (ICPmax/MAP), serum testosterone (T), nitric oxide (NO), and the expression levels of Tie2, AKT, P-AKT, eNOS and P-eNOS in the corpus cavernosa of the penis in each group of rats were measured.

The contents of T、NO and ICPmax/MAP in the penile cavernous tissues of the cast group were significantly lower than the sham group (P< 0.01). After transfection with Tie2 overexpressing lentivirus, the NO content and ICPmax/MAP of the cast+Tie2 group were significantly higher than the cast group (P< 0.01). The expression of Tie2 and P-AKT/AKT and P-eNOS/eNOS in penile cavernous tissue of rats in the cast group were significantly lower than those in the sham group, and the expression of Tie2 and P-AKT/AKT and P-eNOS/eNOS in the cast+Tie2 group were significantly higher than the cast group.

Hypoandrogen may inhibit penile erection by inhibiting the Tie2/AKT/eNOS signaling pathway, reducing the concentration of P-eNOS/eNOS and NO in penile cavernous tissue. Up-regulating the expression of Tie2 in penile cavernous tissue can increase the concentrations of P-AKT/AKT, P-eNOS/eNOS and NO, and improve ED.