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Updated: May 16, 2025

Evaluation of Biomaterials for Bladder Augmentation using Cystometric Analyses in Various Rodent Models
Published on: August 9, 2012
Bladder dysfunction in hypoestrogenic rats with metabolic syndrome can be ameliorated after amniotic fluid stem cell
Ching-Chung Liang1,2, Steven W Shaw2,3,4, Wu-Chiao Hsieh1,2
1Female Urology Section, Department of Obstetrics and Gynecology, Chang Gung Memorial Hospital Linkou Medical Center, Taoyuan 333, Taiwan.
Background:
Bladder dysfunction may occur with high frequency in postmenopausal women with metabolic syndrome (MetS). This study evaluated the therapeutic effects of human amniotic fluid stem cells (hAFSCs) on bladder dysfunction in ovariectomized rats with MetS.
Materials And Methods:
Forty-eight female rats were divided into 4 groups: normal control, ovariectomy (OVX), and OVX and MetS without (OVX + MetS) and with hAFSCs treatment (OVX + MetS + hAFSCs). We assessed cystometric parameters, serum biochemistry parameters, wall thickness of iliac artery, apoptotic cells and collagen volume in bladder tissues, and the expressions of purinergic and muscarinic receptors, apoptosis-associated mitochondrial proteins, and markers of inflammation, fibrosis, and oxidative stress at posttreatment 1 and 3 months.
Results:
OVX + MetS rats showed significant dysfunction of bladder storage, including reduced intercontraction intervals and bladder capacity, along with increased residual urine volume and nonvoiding contractions. There was a significant increase in iliac artery wall thickness, bladder collagen volume, and number of apoptotic cells. Also, there were elevated expressions of P2X3 purinergic and M2/M3 muscarinic receptors, pro-apoptotic proteins, and markers of inflammation, fibrosis, and oxidative stress, with a concurrent decrease in anti-apoptotic protein, Bcl-2. Treatment with hAFSCs helped restoring bladder function, ameliorating histological abnormalities, and reducing pathological markers at 1 and/or 3 months.
Conclusion:
These findings suggest that hAFSCs can effectively mitigate bladder dysfunction in rats with ovarian hormone deficiency and MetS by modulating oxidative stress and mitochondrial apoptotic pathways.

