Synergistic repair of pelvic floor supportive tissues in rats with stress urinary incontinence by electroacupuncture combined with repetitive transspinal magnetic stimulation and mechanisms of action.

Abstract

INTRODUCTION AND HYPOTHESIS: Stress urinary incontinence (SUI), a common condition impacting quality of life, stems frominvoluntary urine leakage due to increased abdominal pressure. Its pathology involves excessive extracellular matrix (ECM)degradation, particularly collagen, in pelvic floor tissues, driven by an imbalance between matrix metalloproteinases (MMPs)and their inhibitors (TIMPs). While electroacupuncture (EA) and repetitive Trans-spinal Magnetic Stimulation (rTSMS) areeach beneficial for SUI, their combined synergistic effects and mechanisms are unexplored. We hypothesized that combinedEA and rTSMS would synergistically repair pelvic floor support structures in SUI rats by modulating the TGF-β1/CTGFsignaling pathway and ECM metabolism. METHODS: An SUI rat model was established and randomly assigned to sham, SUI model, EA, rTSMS, and EA+rTSMSgroups. Treatments were daily for 7 days. Urodynamic parameters (Maximum Bladder Capacity - MBC, Abdominal LeakPoint Pressure - ALPP) were assessed. Histological (Masson's trichrome), immunohistochemical, Western Blot, and qPCRanalyses of anterior vaginal wall tissues evaluated Collagen I/III, TGF-β1, CTGF, MMP1, and TIMP1 expression. RESULTS: Combined EA and rTSMS significantly improved MBC and ALPP in SUI rats, outperforming monotherapy. Histologyshowed ameliorated collagen fiber disorganization. Molecularly, combined therapy significantly upregulated Collagen I/III, TGF-β1, and CTGF, while downregulating MMP1 and upregulating TIMP1, restoring MMP1/TIMP1 balance, comparedto the SUI model group. CONCLUSIONS: This study provides the first evidence of a synergistic effect of combined EA and rTSMS for SUI. This approacheffectively repairs pelvic floor structures and improves urodynamic function by activating TGF-β1/CTGF to promote collagensynthesis and regulating MMP1/TIMP1 to inhibit degradation. This research offers novel evidence and a potentialmechanism for safer, more effective non-invasive SUI treatments.