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Amniotic fluid stem cells ameliorate bladder dysfunction induced by chronic bladder ischemia in rat.
Ching-Chung Liang1,2, Sheng-Wen Steven Shaw1,3, Yi-Hao Lin1,2
1Female Urology Section, Department of Obstetrics and Gynecology, Chang Gung Memorial Hospital Linkou Medical, Taoyuan, Taiwan.
Neurourology and Urodynamics
|June 13, 2017
Summary
Human amniotic fluid-derived stem cells (hAFSCs) treatment improved bladder overactivity and reduced oxidative stress in a rat model of chronic bladder ischemia. This suggests hAFSCs offer a protective effect against ischemia-induced bladder dysfunction.
Area of Science:
- Regenerative Medicine
- Urology
- Cardiovascular Research
Background:
- Atherosclerosis-induced chronic bladder ischemia can lead to bladder overactivity.
- This condition is characterized by impaired bladder function and increased oxidative stress.
Purpose of the Study:
- To investigate the protective effects of human amniotic fluid-derived stem cells (hAFSCs) against bladder overactivity in a rat model.
- To evaluate the impact of hAFSCs on oxidative stress and inflammatory markers in chronic bladder ischemia.
Main Methods:
- Adult female Sprague-Dawley rats underwent arterial balloon endothelial injury (AEI) to induce chronic bladder ischemia.
- Rats received hAFSCs treatment at different time points (1, 3, or 7 days post-AEI).
- Bladder function, iliac artery morphology, and markers of oxidative stress (8OHdG, MDA) and inflammation (TNF-alpha) were assessed.
Main Results:
- Arterial balloon endothelial injury induced bladder overactivity, characterized by decreased voided volumes and increased residual volumes.
- hAFSCs treatment significantly improved bladder overactivity and normalized iliac artery wall thickness.
- Treatment with hAFSCs reduced elevated levels of 8OHdG, MDA, and TNF-alpha, indicating decreased oxidative stress and inflammation.
Conclusions:
- hAFSCs demonstrate a protective effect against bladder overactivity induced by chronic bladder ischemia.
- The therapeutic benefits of hAFSCs are likely mediated by the down-regulation of oxidative stress and TNF-alpha expression.
- hAFSCs represent a potential therapeutic strategy for managing bladder dysfunction associated with chronic ischemia.

