OBJECTIVE: To investigate the effects of botulinum toxin A (BoNT/A) on the expression of nerve growth factor (NGF) and transient receptor potential vanilloid 1 (TRPV1) in the urothelium and detrusor muscle of rats with partial bladder outlet obstruction (BOO)-induced detrusor overactivity. METHODS: Male Sprague-Dawley rats were allocated to a control group, a BOO group, or a BoNT/A-treated BOO group. BoNT/A (1 U) was injected into the detrusor muscle simultaneously with the induction of BOO. The rats were assessed by cystometrography 3 weeks later. The bladder was then removed. Immunofluorescence staining and Western blotting was performed to localize and quantify the expression of NGF and TRPV1 in the urothelium and detrusor muscle. RESULTS: Cystometrography revealed induction of an unstable bladder in the BOO group and recovery of bladder stability after BoNT/A treatment. Expression of the NGF and TRPV1 proteins in the urothelium was significantly greater in the BOO group than in the control group and had decreased significantly with BoNT/A treatment in BOO-induced rat. The expression of NGF in detrusor muscle was significantly greater in the BOO group than in the control group and subsequently decreased significantly with BoNT/A treatment in the BOO-induced rat. In contrast, TRPV1 expression in the detrusor muscle did not differ significantly among the 3 groups. CONCLUSION: Our experiments showed that detrusor wall injection of BoNT/A can modulate the expression of NGF and TRPV1, particularly in the urothelium, in accordance with recovery of bladder function.
OBJECTIVE: To investigate the effects of botulinum toxin A (BoNT/A) on the expression of nerve growth factor (NGF) and transient receptor potential vanilloid 1 (TRPV1) in the urothelium and detrusor muscle of rats with partial bladder outlet obstruction (BOO)-induced detrusor overactivity. METHODS: Male Sprague-Dawley rats were allocated to a control group, a BOO group, or a BoNT/A-treated BOO group. BoNT/A (1 U) was injected into the detrusor muscle simultaneously with the induction of BOO. The rats were assessed by cystometrography 3 weeks later. The bladder was then removed. Immunofluorescence staining and Western blotting was performed to localize and quantify the expression of NGF and TRPV1 in the urothelium and detrusor muscle. RESULTS: Cystometrography revealed induction of an unstable bladder in the BOO group and recovery of bladder stability after BoNT/A treatment. Expression of the NGF and TRPV1 proteins in the urothelium was significantly greater in the BOO group than in the control group and had decreased significantly with BoNT/A treatment in BOO-induced rat. The expression of NGF in detrusor muscle was significantly greater in the BOO group than in the control group and subsequently decreased significantly with BoNT/A treatment in the BOO-induced rat. In contrast, TRPV1 expression in the detrusor muscle did not differ significantly among the 3 groups. CONCLUSION: Our experiments showed that detrusor wall injection of BoNT/A can modulate the expression of NGF and TRPV1, particularly in the urothelium, in accordance with recovery of bladder function.
Authors: Bernadette M M Zwaans; Laura E Lamb; Sarah Bartolone; Heinz E Nicolai; Michael B Chancellor; Stangel-Wójcikiewicz Klaudia Journal: Int Urol Nephrol Date: 2018-08-21 Impact factor: 2.370
Authors: Francis M Hughes; Hayden M Hill; Case M Wood; Andrew T Edmondson; Aliya Dumas; Wen-Chi Foo; James M Oelsen; Goran Rac; J Todd Purves Journal: J Urol Date: 2015-12-18 Impact factor: 7.450