Department of Urology, the Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Department of Urology and Andrology, Peking University Third Hospital, Beijing, China.
Andrology. 2021 Jul;9(4):1264-1274. doi: 10.1111/andr.12995. Epub 2021 Mar 11.
The mechanism of erectile dysfunction (ED) caused by low androgen status is not fully understood.
To investigate whether low androgen status inhibits erectile function of rats by inducing pyroptosis in the corpus cavernosum (CC).
Thirty-six eight-weeks-old healthy male Sprague-Dawley rats were equally divided into six groups: sham-operated group (4w sham, 8w sham), castration group (4w cast, 8w cast), and castration + testosterone (T) group (4w cast + T, 8w cast + T). The rats in castration + T groups were injected with testosterone propionate subcutaneously every other day. After 4 and 8 weeks, the ratio of maximum intracavernous pressure (ICPmax)/mean arterial pressure (MAP), the level of serum T, the concentration of nitric oxide (NO) and interleukin-1β (IL-1β), the expression of NOD-like receptor pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC), Caspase-1 p20, gasdermin D-N (GSDMD-N), transforming growth factor β1 (TGF-β1), collagen-I, and collagen-III, the ratio of smooth muscle/collagen (SM/C), and the proportion of pyroptotic cells in the CC were analyzed.
The ratio of ICPmax/MAP (3/5 V) and SM/C, the level of NO and serum T was significantly decreased in castration groups when compared to other groups (p < 0.01). NLRP3, ASC, Caspase-1, and GSDMD were mainly expressed in the cytoplasm of smooth muscle cells (SMCs) and endothelial cells (ECs) in the CC. The expression of NLRP3, ASC, Caspase-1p20, GSDMD-N, IL-1β, TGF-β1, collagen-I, and collagen-III was significantly increased in castration groups when compared with other groups (p < 0.01). The proportion of pyroptotic cells in the CC was increased significantly in castration groups when compared with other groups (p < 0.05).
Low androgen status inhibits erectile function of rats by promoting CC fibrosis and reducing NO synthesis through pyroptosis of SMCs and ECs in the CC.
低雄激素状态引起的勃起功能障碍（ED）的机制尚未完全阐明。
探讨低雄激素状态是否通过诱导海绵体（CC）细胞焦亡来抑制大鼠的勃起功能。
将 36 只 8 周龄健康雄性 Sprague-Dawley 大鼠等分为 6 组：假手术组（4w 假手术，8w 假手术）、去势组（4w 去势，8w 去势）和去势+睾丸酮（T）组（4w 去势+T，8w 去势+T）。去势+T 组大鼠每隔一天皮下注射丙酸睾酮。4 周和 8 周后，分析最大海绵体压（ICPmax）/平均动脉压（MAP）比值、血清 T 水平、一氧化氮（NO）和白细胞介素-1β（IL-1β）浓度、NOD 样受体含 pyrin 结构域蛋白 3（NLRP3）、凋亡相关斑点样蛋白（ASC）、半胱天冬酶-1 p20、gasdermin D-N（GSDMD-N）、转化生长因子β1（TGF-β1）、胶原-I、胶原-III 的表达、平滑肌/胶原（SM/C）比值以及 CC 中细胞焦亡的比例。
与其他组相比，去势组的 ICPmax/MAP 比值（3/5V）和 SM/C 比值、NO 和血清 T 水平显著降低（p<0.01）。NLRP3、ASC、Caspase-1 和 GSDMD 主要表达于 CC 平滑肌细胞（SMCs）和内皮细胞（ECs）的细胞质中。与其他组相比，去势组的 NLRP3、ASC、Caspase-1p20、GSDMD-N、IL-1β、TGF-β1、胶原-I 和胶原-III 的表达显著增加（p<0.01）。与其他组相比，去势组 CC 中细胞焦亡的比例显著增加（p<0.05）。
低雄激素状态通过促进 CC 纤维化和减少 NO 合成，通过 CC 中 SMCs 和 ECs 的细胞焦亡来抑制大鼠的勃起功能。
