To elucidate the efficacy and underlying mechanisms of postbiotics in ameliorating stress urinary incontinence (SUI) in a rat model.
SUI model was established via pelvic floor injury and bilateral ovariectomy to simulate postmenopausal conditions. Following successful model induction, subjects were randomly allocated into control, model, positive drug, and experimental groups. The positive drug group received midodrine hydrochloride (20 mg/kg), while the experimental group received postbiotics (75 mg/kg) daily for 28 days. Urodynamic and abdominal leak point pressure tests were conducted on days 7, 14, 21, and 28. After 28 days, histopathology and western blot analysis for collagen I (Col I), collagen III (Col III), and elastin, as well as quantitative polymerase chain reaction for gene expression, were performed.
The model group showed abnormal urodynamic waveforms and lower maximum abdominal leak point pressure compared to controls. Histopathology revealed muscle fiber disarray, fiber rupture, and decreased muscle thickness. Both mRNA and protein levels of Col I, Col III, and Elastin were reduced. Midodrine improved urodynamic parameters and pathology, increasing Col I, Col III, and Elastin levels. Postbiotics also improved urodynamic parameters and pathology, with increased protein levels of Col I, Col III, and Elastin, and upregulated mRNA levels of Col I, Col III, Elastin, and transforming growth factor β1.
Postbiotics demonstrate therapeutic potential in alleviating SUI in rats by upregulating the expression of Col I, Col III, Elastin, and transforming growth factor β1 genes, enhancing collagen and elastin protein content in sphincter and pubococcygeus muscles, and consequently restoring muscle contractility and function.