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  • Title: Intravesical botulinum toxin A administration inhibits COX-2 and EP4 expression and suppresses bladder hyperactivity in cyclophosphamide-induced cystitis in rats.
    Author: Chuang YC, Yoshimura N, Huang CC, Wu M, Chiang PH, Chancellor MB.
    Journal: Eur Urol; 2009 Jul; 56(1):159-66. PubMed ID: 18514386.
    Abstract:
    BACKGROUND: Cyclooxygenase 2 (COX-2) elevation and subsequent prostaglandin E(2) (PGE(2)) production play a major role in bladder inflammation and hyperactivity. EP4 receptor, a subtype of PGE(2) receptors, mediates tissue inflammation and hypersensitivity. OBJECTIVE: To investigate the effect of intravesical botulinum toxin A (BoNT-A) on COX-2 and EP4 expression in cyclophosphamide (CYP)-induced cystitis in rats. DESIGN, SETTING, AND PARTICIPANTS: Experimental (N=40) and control animals (N=20) were injected with CYP (75 mg/kg intraperitoneally) or saline on days 1, 4, and 7. BoNT-A (1 ml, 20 unit/ml) or saline were administered into the bladder and retained for 1 h on day 2. INTERVENTION: Waking cystometrograms (CMGs) were performed. Bladder and L6 and S1 spinal cord were harvested on day 8. MEASUREMENTS: CMG parameters, histology, and COX-2 and EP4 expression by immunostaining or western blotting were measured. RESULTS AND LIMITATIONS: CYP induced increased bladder inflammatory reaction, bladder hyperactivity, and COX-2 and EP4 expression in the bladder and spinal cord. The CYP effects were suppressed by BoNT-A treatment. BoNT-A treatment decreased inflammatory reaction (56.5% decrease), COX-2 expression (77.8%, 61.7%, and 54.8% decrease for bladder, L6, and S1 spinal cord, respectively), EP4 expression (56.8%, 26.9%, and 84.2% decrease for bladder, L6, and S1 spinal cord, respectively), and suppressed bladder hyperactivity (intercontraction interval, 107% increase and contraction amplitude, 43% decrease). CONCLUSIONS: CYP injection activated COX2 and EP4 expression in the bladder and spinal cord and induced bladder inflammation and hyperactivity, which effects were suppressed by BoNT-A treatment. These findings suggest a potential benefit of EP4-targeted pharmacotherapy and BoNT-A treatment for bladder inflammatory conditions.
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