Volume 27, Issue 1 (January 2025) 27, 96–100; 10.4103/aja202430
Injectable agents for the induction of Peyronie’s disease in model rats: a comparative study
Du, Guang-Jun1,*; Xing, Si-Yan1,2,*; Wu, Ning1; Wang, Tong1; Jiang, Yue-Hui1; Song, Tao1; Yang, Bai-Bing1; Dai, Yu-Tian1
1Department of Andrology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing 210008, China
2Department of Andrology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School of Nanjing Medical University, Suzhou 210008, China
Correspondence: Dr. YT Dai (yutian_dai@nju.edu.cn) or Dr. BB Yang (baibing.yang@njglyy.com)
Originally published: August 13, 2024 Received: November 21, 2023 Accepted: April 25, 2024
Abstract |
Peyronie’s disease (PD) is a disorder characterized by fibrous plaque formation in the penile tissue that leads to curvature and complications in advanced stages. In this study, we aimed to compare four injectable induction agents for the establishment of a robust rat model of PD: transforming growth factor-β1 (TGF-β1), fibrin, sodium tetradecyl sulfate (STS) combined with TGF-β1, and polidocanol (POL) combined with TGF-β1. The results showed that injection of TGF-β1 or fibrin into the tunica albuginea induced pathological endpoints without causing penile curvature. The STS + TGF-β1 combination resulted in both histological and morphological alterations, but with a high incidence of localized necrosis that led to animal death. The POL + TGF-β1 combination produced pathological changes and curvature comparable to STS + TGF-β1 and led to fewer complications. In conclusion, fibrin, STS + TGF-β1, and POL + TGF-β1 all induced PD with a certain degree of penile curvature and histological fibrosis in rats. The POL + TGF-β1 combination offered comparatively greater safety and clinical relevance and may have the greatest potential for PD research using model rats.
Keywords: fibrin; Peyronie’s disease; polidocanol; rat model; sodium tetradecyl sulfate; TGF-β1
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