Chen Li, Ziyu Wang, Guang Yue, Han Deng, Limin Liao, Linquan Jin, Xing Li
PFES effectively repairs pelvic floor muscle structure and function by reducing muscle edema and fiber disruption. This effect may be associated with up‑regulation of type I and III collagens to facilitate ECM remodeling, induction of VEGF mediated angiogenesis, and down‑regulation of FBXO32 to counteract muscle atrophy. These findings elucidate PFES mechanisms and support its clinical application.
PURPOSE: This study aimed to investigate the imaging characteristics and molecular mechanisms by which pelvic floor electrical stimulation (PFES) improves pelvic floor muscle injury in a rat model of stress urinary incontinence (SUI).
METHODS: An SUI model was established in female Sprague‑Dawley rats via vaginal distension combined with bilateral ovariectomy. One week post‑modeling, the stimulation group received intravaginal PFES for 2 weeks. Evaluations included 9.4 T MRI, urodynamic tests, histopathological staining, qPCR, Western blotting, and RNA‑seq.
RESULTS: PFES significantly elevated ALPP compared with controls, indicating improved urinary continence. MRI demonstrated that PFES attenuated focal hyperintensity, muscle edema, and fiber disorganization in the pubococcygeus muscle. Histological analyses confirmed that PFES restored dense muscle fiber arrangement and collagen distribution, and immunohistochemistry showed upregulated expression of COL1A1, COL3A1, and CD34. RNA‑seq revealed that differentially expressed genes were prominently enriched in ECM organization, focal adhesion, ECM-receptor interaction, and the PI3K-Akt pathway. Western blotting verified that PFES increased COL1A1, COL3A1, and VEGFA, while suppressing the atrophy‑related ubiquitin ligase FBXO32.
CONCLUSION: PFES effectively repairs pelvic floor muscle structure and function by reducing muscle edema and fiber disruption. This effect may be associated with up‑regulation of type I and III collagens to facilitate ECM remodeling, induction of VEGF mediated angiogenesis, and down‑regulation of FBXO32 to counteract muscle atrophy. These findings elucidate PFES mechanisms and support its clinical application.