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Structural and functional abnormalities of penile cavernous endothelial cells result in erectile dysfunction at experimental autoimmune prostatitis rat.
Journal of Inflammation ( IF 4.4 ) Pub Date : 2019-07-25 , DOI: 10.1186/s12950-019-0224-0
Tianrun Huang 1 , Guangchun Wang 1 , Yangyang Hu 1 , Heng Shi 1 , Keyi Wang 1 , Lei Yin 1 , Bo Peng 1
Affiliation  

Background 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. Methods 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. Results 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. Conclusion 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.

中文翻译:

阴茎海绵状内皮细胞的结构和功能异常导致实验性自身免疫性前列腺炎大鼠勃起功能障碍。

背景 越来越多的人认识到 CP/CPPS 与 ED 的关联。然而,具体的作用机制仍不清楚。本研究的目的是研究 EAP 大鼠海绵状内皮细胞的结构和功能异常,这可能导致 ED。方法采用大鼠前列腺蛋白提取物辅以免疫佐剂诱导大鼠EAP,测定ICP和MAP,检测海绵体炎症因子浸润、Akt、eNOS、AR、nNOS和iNOS。随后,通过MACS纯化正常大鼠和EAP大鼠海绵体内皮细胞,并评估代谢、氧化应激、MMP、Akt、eNOS、AR和iNOS。结果EAP大鼠模型构建成功。EAP大鼠最大ICP/MAP比值明显低于正常大鼠,海绵体TNF-α浸润明显高于正常大鼠。此外,Akt、eNOS和AR均降低,iNOS显着升高。EAP大鼠阴茎海绵体内皮细胞的生长和代谢减少,炎症因子mRNA增加,细胞内氧化应激也显着增加。EAP大鼠海绵体内皮细胞MMP降低,Akt、eNOS、AR表达也明显降低,iNOS明显升高。结论前列腺局部炎症浸润,促进细胞因子浸润海绵体,引起氧化应激增加,代谢或MMP减少。此外,AR,
更新日期:2020-04-22
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