Chronic inflammation is thought to be a major causative factor for the development of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS). Tadalafil, a phosphodiesterase type 5 inhibitor (PDE5-I), which has been used for the treatment of BPH-LUTS in daily practice, is known to act at several urinary organs. In this study, focused on the prostate, we examined the effect of tadalafil on the pathological changes and inflammatory factors in a rat nonbacterial prostatitis (NBP) model. Forty ten-month-old male Wistar rats were divided into nonbacterial prostatitis (NBP), NBP with tadalafil treatment (NBP-tadalafil), control, and control treated with tadalafil (control-tadalafil) groups (n = 10 per group). The NBP and NBP-tadalafil groups were castrated and then received daily subcutaneous 17β-estradiol for 30 days. The control-tadalafil and NBP-tadalafil groups were administered daily oral tadalafil for 30 days. All rats were then sacrificed and pathological changes and inflammatory factors were assessed in the prostatic tissues. In the NBP group, the stroma-to-epithelium (S/E) ratio in the ventral prostate was significantly higher than in the control group (P < 0.001). In the NBP-tadalafil group, the S/E ratio was significantly lower than in the NBP group (P < 0.001). The macrophage levels and the extent of T-cell infiltration in the NBP-tadalafil group were significantly lower than in the NBP group (P < 0.005; P < 0.001, respectively). Compared with the NBP group, tissue concentrations of inflammatory cytokines, such as tumor necrosis factor-α, interleukin-8, and interleukin-1β, were significantly downregulated in the NBP-tadalafil group (P < 0.01; P < 0.05; P < 0.005, respectively). Tadalafil suppressed stromal predominance and showed anti-inflammatory effects in a rat NBP model in association with downregulation of inflammatory cytokines.

中文翻译：

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磷酸二酯酶 5 抑制剂他达拉非可抑制非细菌性前列腺炎大鼠模型中的基质优势和炎症


慢性炎症被认为是良性前列腺增生（BPH）和下尿路症状（LUTS）发生的主要致病因素。他达拉非是一种 5 型磷酸二酯酶抑制剂 (PDE5-I)，在日常实践中已用于治疗 BPH-LUTS，已知可作用于多个泌尿器官。在本研究中，我们以前列腺为重点，在大鼠非细菌性前列腺炎（NBP）模型中检查了他达拉非对病理变化和炎症因子的影响。将40只10月龄雄性Wistar大鼠分为非细菌性前列腺炎（NBP）组、NBP加他达拉非治疗组（NBP-他达拉非）、对照组和他达拉非治疗对照组（对照-他达拉非）组（每组n = 10）。 NBP和NBP-他达拉非组被阉割，然后每天皮下注射17β-雌二醇，持续30天。对照他达拉非组和NBP他达拉非组每天口服他达拉非，持续30天。然后处死所有大鼠并评估前列腺组织的病理变化和炎症因子。在 NBP 组中，前列腺腹侧的基质与上皮 (S/E) 比率显着高于对照组 (P < 0.001)。在 NBP-他达拉非组中，S/E 比显着低于 NBP 组 (P < 0.001)。 NBP-他达拉非组的巨噬细胞水平和 T 细胞浸润程度显着低于 NBP 组（分别为 P < 0.005；P < 0.001）。与NBP组相比，NBP-他达拉非组的炎症细胞因子，如肿瘤坏死因子-α、白细胞介素-8和白细胞介素-1β的组织浓度显着下调（P < 0.01；P < 0.05；P < 0.005，分别）。 他达拉非在大鼠 NBP 模型中抑制基质优势并显示出与炎症细胞因子下调相关的抗炎作用。