The relationship between chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and erectile dysfunction (ED) has been shown in many studies. However, the specific mechanism remains unclear. This study was to investigate the corpus cavernosum smooth muscle cell function and phenotype transformation in Experimental autoimmune prostatitis (EAP) rats. EAP was induced in rats by using prostate protein supplemented with immuneadjuvant extraction, and the max-ICP and MAP were measured. IHC and Masson staining were done to assess inflammatory infiltration and collagen deposition in the corpus cavernosum, respectively. Subsequently, normal rat and EAP rat CCSMCs were purified by tissue block implantation and differential adherence method. The oxidative stress, smooth muscle phenotype transformation, cell cycle and intracellular calcium ion transport were also evaluated. The ratio of max ICP/MAP in EAP rats significantly reduced, and the TNF-α content and collagen deposition in the corpus cavernosum markedly increased as compared to healthy rats. High-purity rat CCSMCs were obtained. Oxidative stress was evident and the cGMP content decreased in the EAP rat CCSMCs. The expression of Cav1.2, IP3R1 and RyR2 increased, but the SERCA2 expression decreased in EAP rat CCSMCs, which was accompanied by increased intracellular calcium. Increased expression of OPN, collagen and KCa3.1, decreased Calponin expression and increased proportion of cells in the S phase were also observed in the EAP rat CCSMCs. CP causes oxidative stress and imbalance of intracellular calcium in CCSMCs and promotes CCSMCs transformation from contractile to synthetic state, which may be involved in the pathogenesis of ED.

中文翻译：

---

慢性前列腺炎/慢性盆腔痛综合征前列腺炎大鼠阴茎海绵体平滑肌细胞功能障碍及表型转化与勃起功能障碍有关

许多研究表明慢性前列腺炎/慢性盆腔疼痛综合征 (CP/CPPS) 与勃起功能障碍 (ED) 之间的关系。然而，具体机制仍不清楚。本研究旨在研究实验性自身免疫性前列腺炎（EAP）大鼠的海绵体平滑肌细胞功能和表型转化。用添加免疫佐剂提取物的前列腺蛋白诱导大鼠EAP，并测量max-ICP和MAP。进行 IHC 和 Masson 染色以分别评估海绵体中的炎症浸润和胶原沉积。随后，通过组织块植入和差示粘附法纯化正常大鼠和EAP大鼠CCSMC。氧化应激、平滑肌表型转化、还评估了细胞周期和细胞内钙离子转运。与健康大鼠相比，EAP大鼠最大ICP/MAP比值显着降低，海绵体TNF-α含量和胶原沉积显着增加。获得高纯度大鼠CCSMCs。EAP大鼠CCSMCs氧化应激明显，cGMP含量降低。EAP大鼠CCSMCs中Cav1.2、IP3R1和RyR2表达升高，SERCA2表达降低，并伴有细胞内钙离子升高。在 EAP 大鼠 CCSMCs 中也观察到 OPN、胶原蛋白和 KCa3.1 的表达增加，Calponin 表达降低和 S 期细胞比例增加。CP引起CCSMCs氧化应激和细胞内钙失衡，促进CCSMCs从收缩状态向合成状态转变，