Huang Tianrun, Wang Guangchun, Hu Yangyang, Shi Heng, Wang Keyi, Yin Lei, Peng Bo
Department of Urology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, NO 301 Yanchang Road, Shanghai, 200072 People's Republic of China.
J Inflamm (Lond). 2019 Jul 25;16:20. doi: 10.1186/s12950-019-0224-0. eCollection 2019.
There 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.
we 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.
The 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.
The 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.
慢性前列腺炎/慢性骨盆疼痛综合征(CP/CPPS)与勃起功能障碍(ED)之间的关联日益受到关注。然而,其具体作用机制仍不清楚。本研究旨在探讨实验性自身免疫性前列腺炎(EAP)大鼠海绵体内皮细胞的结构和功能异常,这可能导致ED。
我们用大鼠前列腺蛋白提取物辅以免疫佐剂诱导EAP大鼠,测量其阴茎海绵体内压(ICP)和平均动脉压(MAP),并检测海绵体内炎性因子浸润情况以及蛋白激酶B(Akt)、内皮型一氧化氮合酶(eNOS)、雄激素受体(AR)、神经元型一氧化氮合酶(nNOS)和诱导型一氧化氮合酶(iNOS)。随后,通过磁珠分选法(MACS)纯化正常大鼠和EAP大鼠的海绵体内皮细胞,并评估其代谢、氧化应激、基质金属蛋白酶(MMP)、Akt、eNOS、AR和iNOS。
成功构建了EAP大鼠模型。EAP大鼠的最大ICP/MAP比值显著低于正常大鼠,海绵体内肿瘤坏死因子-α(TNF-α)浸润显著高于正常大鼠。此外,Akt、eNOS和AR减少,iNOS显著增加。EAP大鼠海绵体内皮细胞的生长和代谢降低,炎性因子mRNA增加,细胞内氧化应激也显著增加。EAP大鼠海绵体内皮细胞的MMP降低,Akt、eNOS和AR的表达也显著降低,iNOS显著增加。
前列腺发生局部炎症浸润,促使细胞因子浸润到海绵体,导致氧化应激增加,代谢或MMP降低。此外,AR、Akt和eNOS的表达及磷酸化也降低,从而抑制海绵体的舒张功能,导致勃起功能下降。