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Stress urinary incontinence (SUI) animal model
Stress urinary incontinence (SUI) animal model
Publish an article
Stress urinary incontinence
Introduction to the SUI Animal Model
Stress urinary incontinence (SUI) is a condition characterized by involuntary urine leakage that occurs during activities that increase intra-abdominal pressure, such as coughing, sneezing, or physical exertion. It is often associated with impaired urethral sphincter function, damage to the pelvic floor support structures, and neurological abnormalities. Animal models of SUI are primarily established by replicating pathological processes such as pelvic floor tissue laxity, urethral sphincter injury, or nerve damage. These models typically exhibit features including reduced leak point pressure (LPP), decreased urethral closure pressure, and structural alterations in the sphincter tissue, thereby effectively mimicking the onset and progression of postpartum and age‑related stress urinary incontinence in humans.
SUI Animal Model Platform Service Advantages of Aniphe BioLab
Aniphe BioLab has established a comprehensive animal model platform for stress urinary incontinence (SUI), offering multiple modeling approaches and systematic efficacy evaluation services tailored to diverse research needs, thereby providing robust preclinical support for studies on the pathogenesis of SUI and the development of innovative therapies.
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Modeling is stable and reliable. Standardized operating procedures ensure a high model success rate, with good concordance between the urinary incontinence phenotype and urethral functional impairment. |
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The evaluation system has been improved. It is possible to conduct multidimensional assessments, including stress urinary incontinence pressure measurements, urodynamic studies, histopathology, and molecular biology analyses. |
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Research on the compatibility of multiple therapies Supports efficacy validation for drugs, stem cells, exosomes, biomaterials, and tissue-engineered products. |
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Extensive project experience We offer end-to-end services, from model development and sample analysis to data interpretation, providing clients with high-quality preclinical research solutions. |
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The filament occlusion method (MCAO) is used to establish the model, which avoids craniotomy, minimizes animal trauma, and yields highly reproducible results. |
Standardized surgical protocols, combined with an experienced technical team, ensure the stability and consistency of model creation. |
The Longa score and the Bederson score, combined with TTC staining, were used to comprehensively validate the model’s phenotype. |
Retain photographs of key procedural milestones and original records to ensure traceability of the experimental process. |
A standardized in vivo solution that meets the needs of cerebral ischemia mechanism research and drug efficacy evaluation. |
| Modeling cycle | 4–8 weeks |
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SD rats, New Zealand rabbits |
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Pharmacologic agents: duloxetine (increases the urethral closure pressure), phenylephrine (an α‑agonist). |
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Neuro‑muscular mechanisms underlying SUI induced by childbirth and aging; regenerative evaluation of sphincter repair using stem cells and hydrogels; pharmacological screening for agents—administered orally or locally—that enhance urethral closure pressure; preclinical optimization of physical therapies (magnetic/electrical stimulation) and pelvic floor reconstruction surgery. |
Construction of the SUI animal model
A stress urinary incontinence (SUI) model was established by combining ovariectomy with vaginal balloon traction. First, bilateral ovariectomy (OVX) was performed on adult female mice or rats to reduce circulating estrogen levels, thereby mimicking the postmenopausal decline in pelvic floor support. Following a recovery period of 2–4 weeks, a custom‑designed balloon catheter was inserted into the vagina and maintained under continuous inflation and traction for a specified duration, mechanically compressing and stretching the pelvic floor to simulate the muscle, connective tissue, and neural injuries incurred during childbirth. Post‑modeling, animals exhibit hallmark SUI phenotypes, including reduced leak point pressure (LPP), impaired urethral closure, and structural damage to pelvic floor tissues. This model integrates both postmenopausal estrogen deficiency and obstetric trauma—two key pathogenic factors—and closely resembles the clinical pathogenesis of stress urinary incontinence in women. It is widely employed for investigating SUI pathophysiology and for evaluating the efficacy of pharmacological agents, stem cell therapies, and tissue‑engineering approaches.
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