Testosterone is overwhelmingly important in regulating erectile physiology. However, the associated molecular mechanisms are poorly understood. The purpose of this study was to explore the effects and mechanisms of testosterone in erectile dysfunction (ED) in castrated rats. Forty male Sprague-Dawley rats were randomized to four groups (control, sham-operated, castration and castration-with-testosterone-replacement). Reactive oxygen species (ROS) production was measured by dihydroethidium (DHE) staining. Erectile function was assessed by the recording of intracavernous pressure (ICP) and mean arterial blood pressure (MAP). Protein expression levels were examined by western blotting. We found that castration reduced erectile function and that testosterone restored it. Nitric oxide synthase (NOS) activity was decrease in the castrated rats, and testosterone administration attenuated this decrease (each p < 0.05). The testosterone, dihydrotestosterone, cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) concentrations were lower in the castrated rats, and testosterone restored these levels (each p < 0.05). Furthermore, the cyclooxygenase-2 (COX-2) and prostacyclin synthase (PTGIS) expression levels and phospho-endothelial nitric oxide synthase (p-eNOS, Ser1177)/endothelial nitric oxide synthase (eNOS) ratio were reduced in the castrated rats compared with the controls (each p < 0.05). In addition, the p40phox and p67phox expression levels were increased in the castrated rats, and testosterone reversed these changes (each p < 0.05). Overall, our results demonstrate that testosterone ameliorates ED after castration by reducing ROS production and increasing the activity of the eNOS/cGMP and COX-2/PTGIS/cAMP signaling pathways.
Varicocele is the most common cause of male infertility. Varicoceles are classified into two types: clinical and subclinical varicoceles. Some researchers reported right subclinical varicoceles are often accompanied with left clinical varicoceles. However, the treatment is controversial. Our aim was to compare the clinical outcome of unilateral varicocelectomy (UV) and bilateral varicocelectomy (BV) in infertile males with left clinical and right subclinical varicocele. A total of four randomised controlled trials (RCT) were enrolled in this study, including 637 cases with left clinical and right subclinical varicocele (318 cases in the BV group and 319 cases in the UV group). The fixed effects model combined difference in progressive sperm motility between the two groups was 6.42% (95% CI: 5.09, 7.75). The random effects model combined difference in normal sperm morphology between the two groups was 2.04% (95% CI: 0.60, 3.48). The odds ratio shown by the fixed effects model in spontaneous pregnancy rate was 1.73 (95% CI: 1.24, 2.43). No statistically significant difference between the two groups was found in sperm concentration and sperm motility. Thus, BV may be superior to UV for infertile male patients with left clinical and right subclinical varicocele. However, more properly conducted RCTs are still needed.
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