Published online May 26, 2022. doi: 10.4252/wjsc.v14.i5.330
Peer-review started: October 26, 2021
First decision: December 4, 2021
Revised: January 3, 2022
Accepted: April 25, 2022
Article in press: April 25, 2022
Published online: May 26, 2022
Processing time: 211 Days and 21.6 Hours
Diabetes mellitus (DM) is a serious and growing global health burden. It is estimated that 80% of diabetic patients have micturition problems such as poor emptying, urinary incontinence, urgency, and urgency incontinence. Patients with diabetic bladder dysfunction are often resistant to currently available therapies. It is necessary to develop new and effective treatment methods.
Exogenous insulin has been used to prevent various complications of DM, but almost all patients will eventually have complications. Stem cells have recently demonstrated efficacy in preclinical studies of diabetic bladder dysfunction. Human amniotic fluid stem cells (hAFSCs) can be obtained from amniotic fluid, easy to culture, and phenotypically and genetically stable, suggesting that these stem cells can be used as a novel source of cell therapy.
The present study aimed to investigate the effect of hAFSCs therapy and whether the therapeutic effect could be similar to that of insulin treatment on bladder dysfunction using a type 2 DM rat model.
Sixty female Sprague-Dawley rats were divided into five groups: Group 1, normal-diet control (control); group 2, high-fat diet (HFD); group 3, HFD plus streptozotocin (STZ)-induced hyperglycemia like-DM (DM); group 4, DM plus insulin treatment (DM + insulin); group 5, DM plus hAFSCs injection via the tail vein (DM + hAFSCs). Conscious cystometric studies were done at 4 and 12 wk after insulin treatment or 3 × 106 hAFSCs therapy. Immunoreactivities and mRNA expression of bladder muscarinic receptors, nerve growth factor (NGF), sensory nerve markers, insulin, MafA, and pancreatic-duodenal homeobox-1 (PDX-1) in pancreatic beta cells were studied.
Compared with DM rats, insulin but not hAFSCs treatment could reduce the bladder weight and improve the voided volume, intercontraction interval, bladder capacity, and residual volume. However, both insulin and hAFSCs treatment could help regain the blood glucose and bladder functions to the levels near controls. The immunoreactivities and mRNA expression of M2- and M3-muscarinic receptor (M2 and M3) were increased mainly at 4 wk, while the number of beta cells in islets and the immunoreactivities and/or mRNA expression of NGF, calcitonin gene-related peptide (CGRP), substance P, insulin, MafA, and PDX-1 were decreased in DM rats. However, both insulin and hAFSCs treatment could help regain the expression of M2, M3, NGF, CGRP, substance P, MafA, and PDX-1 to near the levels of controls at 4 and/or 12 wk.
Although insulin but not hAFSCs therapy can recover the bladder dysfunction caused by type 2 DM, both insulin and hAFSCs therapy can help regain the bladder function to near the levels of control.
In the STZ-induced diabetic rat model, hAFSCs therapy could help regain bladder function and may serve as an alternative treatment for diabetic bladder dysfunction. Our study highlights the potential of hAFSCs for cell replacement and regeneration therapy for DM.