Abstract
BackgroundThere is growing recognition of the association of CP/CPPS accompany with ED. However, the specific mechanism of action remains unclear. The aim of this study was to investigate structural and functional abnormalities of cavernous endothelial cells in EAP rat, which may result in the ED.Methodswe use rat prostate protein extract supplemented with immunoadjuvant to induce EAP rat, ICP and MAP were measured and inflammatory factor infiltration, Akt, eNOS, AR, nNOS and iNOS in the corpus cavernosum were tested. Subsequently, the normal rat and EAP rat cavernosum endothelial cells were purified by MACS, and the metabolism, oxidative stress, MMP, Akt, eNOS, AR and iNOS were evaluated.ResultsThe EAP rat model was successfully constructed. The ratio of max ICP/MAP in EAP rat was significantly lower and TNF-α infiltration in corpus cavernosum was significantly higher than normal rats. Besides, Akt, eNOS and AR were decreased, iNOS was significantly increased. The growth and metabolism of endothelial cells in the EAP rats corpus cavernosum decreased and inflammatory factor mRNA was increased and intracellular oxidative stress was also increased significantly. The MMP of EAP rats cavernosum endothelial cells decreased and the expression of Akt, eNOS and AR were also significantly decreased, iNOS was significantly increased.ConclusionThe prostate suffer local inflammatory infiltrate and promotes cytokines infiltrated into corpus cavernosum caused the oxidative stress increases and the metabolism or MMP decreases. In addition, AR, Akt and eNOS expression and phosphorylation are also reduced, thereby inhibiting the diastolic function of the corpus cavernosum, resulting in decreased erectile function.
Highlights
Prostatitis is the most common urinary system disease in men under 50 years of age [1]
Effect of CP/Chronic prostatitis/chronic pelvic pain syndrome (CPPS) on erectile function in rats No statistically significant difference was observed in the total body weight as well as the penis weight among experimental autoimmune prostatitis (EAP) rats and controls
We reported endothelial nitric oxide synthase (eNOS) was decreased significantly both in EAP rat corpus cavernosum and corpus cavernosum endothelial cells combined with lower max intracavernous pressure (ICP)/ mean systemic arterial pressure (MAP) ratio
Summary
Prostatitis is the most common urinary system disease in men under 50 years of age [1]. The clinical manifestations of prostatitis are complex and diverse. Symptoms such as Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) are the most common. Along the inner aspect of the tunica albuginea, flattened columns or sinusoidal trabeculae composed of fibrous tissue and smooth muscle surround the endothelial-lined sinusoids (cavernous spaces) [7, 8]. The release of NO increases the production of cyclic guanosine monophosphate (cGMP), which relaxes cavernosal smooth muscle, leading to arterial inflow increase and the sinusoids within the corpora cavernosa distend with blood. Shoskes et al found that prostatitis can lead to arterial stiffness associated with NO-mediated endothelial dysfunction [9]. Whether prostatitis damage to the corpus cavernosum endothelial cells could causes ED are still unclear. The aim of this study was to investigate structural and functional abnormalities of cavernous endothelial cells in EAP rat, which may result in the ED
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