Muscle-Derived Stem Cells Alleviate Voiding Dysfunction and Urethral Injury in Rats with Stress Urinary Incontinence through TGF-β1/CTGF Signaling Pathway
Objective To investigate the effects of muscle-derived stem cells(MDSCs)on voi-ding dysfunction and urethral injury in rats with stress urinary incontinence(SUI)based on trans-forming growth factor β1/connective tissue growth factor(TGF-β1/CTGF)signaling pathway.Methods MDSCs were isolated and cultured,and the expression of Desmin and Sca-1 were detec-ted by immunocytochemistry.A total of 40 female SD rats were randomly allocated to four groups:NC group(rats with no treatment),SUI group(rats with SUI),MDSCs group(SUI rats treated with MDSCs),and MDSCs+SB431542 group(SUI rats treated with MDSCs and TGF-β1/CTGF signaling inhibitor SB431542),with 10 rats in each group.The positive rate of sneezing test,maximum bladder volume(MBC),leak point pressure(LPP),abdominal leak point pressure(ALPP),urine output,residual urine output,and voiding efficiency were compared between the four groups.The histopathological changes of urethra were observed by HE staining,and the ex-pression of TGF-β1 and CTGF proteins in urethral tissues were detected by Western blotting.Re-sults The MDSCs with Desmin and Sca-1 expression were successfully obtained.Compared with the NC group,the SUI rats showed an increase in positive rate of sneezing test,MBC,LPP,AL-PP,urine output and residual urine output,a decrease in voiding efficiency and TGF-β1 and CTGF expression,and severe urethral injury(P<0.05).Compared with the SUI group,MDSCs reduced the positive rate of sneezing test,MBC,LPP,ALPP,urine output and residual urine output,en-hanced the voiding efficiency and TGF-β1 and CTGF expression,and relieved urethral injury(P<0.05).Compared with the MDSCs group,SB431542 treatment increased the positive rate of snee-zing test,MBC,LPP,ALPP,urine output and residual urine output,reduced the voiding efficiency and TGF-β1 and CTGF expression,and aggravated urethral injury(P<0.05).Conclusion MDSCs can improve voiding function and alleviate urethral injury in rats with SUI through regulating TGF-β1/CTGF signaling pathway.