Background The number of erectile dysfunction (ED) patients is increasing annually. How to improve the effectiveness of ED treatment is an important issue for the field of andrology. Objectives To investigate whether low androgen status impairs the erectile function of rats by regulated endothelial nitric oxide synthase (eNOS) uncoupling. Materials and methods Thirty‐six 8‐week‐old male Sprague Dawley (SD) rats were randomly divided into six groups as follows: 4‐week sham‐operated group (4w‐sham), 4‐week castration group (4w‐cast), 4‐week castration + testosterone (T) group (4w‐cast + T), 8‐week sham‐operated group (8w‐sham), 8‐week castration group (8w‐cast), and 8‐week castration + T group (8w‐cast + T). Three mg/kg of T was subcutaneously injected every other day in castration + T groups. The ratio of the maximum intracavernous pressure/the mean arterial pressure (ICPmax/MAP), the level of serum T, dihydrobiopterin(BH2), tetrahydrobiopterin (BH4), nitric oxygen(NO), 3‐nitrotyrosine(3NT), dihydrofolate reductase (DHFR), guanosine triphosphate cyclohydrolase 1 (GTPCH1), nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2), and eNOS monomers/dimers in the corpus cavernosum were detected. Results The ratio of ICPmax/MAP and BH4/BH2, the level of serum T, NO, and GTPCH1 decreased significantly in castration groups compared with sham‐operated groups and castration + T groups (P < .05) and decreased significantly in 8w‐cast group compared with 4w‐cast group (P < .05). The expression of 3NT and NOX2 and the ratio of eNOS monomers/dimers increased significantly in castration groups compared with sham‐operated groups and castration + T groups (P < .01) and increased significantly in 8w‐cast group compared with 4w‐cast group (P < .01). The expression of DHFR in 4w‐cast group was significantly higher than that in 4w‐sham group and 4w‐cast + T group (P < .01) and in 8w‐cast group was significantly lower than that in 8w‐sham group and 8w‐cast + T group (P < .01). Discussion and Conclusion Low androgen status induces eNOS uncoupling by reducing BH4/BH2 and increasing 3NT. Due to the decreased NO production, the erectile function of the rats was impaired.
Hao-Zhou Yang and Wen-ju Xiong equally contributed to this study.
Background The relationship between galanin and erectile function under low androgen levels is still unclear. Aim To explore whether a low testosterone level damages the erection of a rat by regulating the expression of galanin and GalR in penile cavernous tissue. Methods Thirty-six male Sprague-Dawley rats, 8 weeks of age, were randomly grouped as follows (n = 6): control, castration, castration + testosterone replacement, control + transfection, castration + transfection, and castration + empty transfection. At 4 weeks after castration, rats in the transfection group were injected with lentivirus carrying the targeting galanin gene (2 × 108 TU/mL, 10 μL) in the corpus cavernosum. After 1 week of injection, the intracavernosal pressure (ICP), mean arterial blood pressure (MAP), nitric oxide (NO), serum testosterone concentration, galanin, GalR1-3, ROCK1, ROCK2, and p-eNOS/eNOS in the rat penile tissues were evaluated. Outcomes ICPmax/MAP and the expression of galanin in the corpus cavernosum in castrated rats were obviously decreased as compared with those in the control rats. Results The castrated rats showed remarkably lower ICPmax/MAP, galanin, GalR1-3, p-eNOS/eNOS, and NO content and markedly higher ROCK1 and ROCK2 in penile tissues than the control group (P < .05). The transfected rats administrated with LV Gal had obviously higher ICPmax/MAP, p-eNOS/eNOS, and NO content and less ROCK1 and ROCK2 protein expression in the corpus cavernosum when compared with the castration group (P < .05). Clinical Translation Upregulating the expression of galanin in the penile corpus cavernosum might be a novel method of treating erectile dysfunction caused by a low androgen level. Strengths and Limitations The conclusions obtained in the animal experiments need to be confirmed in human data. Conclusion The erectile function of hypoandrogen rats might be inhibited by downregulating the level of galanin and GalR1-3, upregulating ROCK1 and ROCK2 levels, and inhibiting the eNOS/NO signaling pathway in penile corpus cavernosum.
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