Caveolin-1 scaffolding domain-derived peptide enhances erectile function by regulating oxidative stress, mitochondrial dysfunction, and apoptosis of corpus cavernosum smooth muscle cells in rats with cavernous nerve injury.

Autor: Xi Y; Department of Urology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510000, China., Feng Z; Department of Urology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510000, China., Xia T; Department of Urology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510000, China., Hong Y; Department of Urology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510000, China., Wu J; Department of Urology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510000, China., Chen J; Department of Urology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510000, China., Ge Y; Department of Urology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510000, China; Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230000, China. Electronic address: geylong3@mail2.sysu.edu.cn., Xiao H; Department of Urology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510000, China. Electronic address: xiaohjun@mail.sysu.edu.cn.
Jazyk: angličtina
Zdroj: Life sciences [Life Sci] 2024 Jul 01; Vol. 348, pp. 122694. Date of Electronic Publication: 2024 May 06.
DOI: 10.1016/j.lfs.2024.122694
Abstrakt: Aim: Increased corpus cavernosum smooth muscle cells (CCSMCs) apoptosis in the penis due to cavernous nerve injury (CNI) is a crucial contributor to erectile dysfunction (ED). Caveolin-1 scaffolding domain (CSD)-derived peptide has been found to exert potential antiapoptotic properties. However, whether CSD peptide can alleviate CCSMCs apoptosis and ED in CNI rats remains unknown. The study aimed to determine whether CSD peptide can improve bilateral CNI-induced ED (BCNI-ED) by enhancing the antiapoptotic processes of CCSMCs.
Main Methods: Fifteen 10-week-old male Sprague-Dawley (SD) rats were randomly classified into three groups: sham surgery (Sham) group and BCNI groups that underwent saline or CSD peptide treatment respectively. At 3 weeks postoperatively, erectile function was assessed and the penis tissue was histologically examined. Furthermore, an in vitro model of CCSMCs apoptosis was established using transforming growth factor-beta 1 (TGF-β1) to investigate the mechanism of CSD peptide in treating BCNI-ED.
Key Findings: In BCNI rats, CSD peptide significantly prevented ED and decreased oxidative stress, the Bax/Bcl-2 ratio, and the levels of caspase3. TGF-β1-treated CCSMCs exhibited severe oxidative stress, mitochondrial dysfunction, and apoptosis. However, CSD peptide partially reversed these alterations.
Significance: Exogenous CSD peptide could improve BCNI-ED by inhibiting oxidative stress, the Bax/Bcl-2 ratio, and caspase3 expression in penile tissue. The underlying mechanism might involve the regulatory effects of CSD peptide on oxidative stress, mitochondrial dysfunction, and apoptosis of CCSMCs following CNI. This study highlights CSD peptide as an effective therapy for post-radical prostatectomy ED (pRP-ED).
Competing Interests: Declaration of competing interest The authors declare no conflict of interest.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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