Effects of intravesical instillation of cyclooxygenase‐2 inhibitor on the expression of inducible nitric oxide synthase and nerve growth factor in cyclophosphamide‐induced overactive bladder

Abstract

stained immunohistochemically for iNOS and NGF. RESULTSIn the OAB rats, the contraction interval and intercontraction interval were significantly shorter than in control rats, and the contraction time and pressure were significantly greater. In the COX-2 inhibitortreated rats, the contraction interval and intercontraction interval were significantly longer than in the OAB rats, and the contraction time was significantly shorter. On immunohistochemical staining, there was no iNOS activity and NGF activity was minimally localized in the mucosa and submucosa in the control group. In the OAB rats, NGF activity in the mucosa and submucosa were increased, and there was greater expression of iNOS in all layers and of NGF in detrusor; in the COX-2 inhibitor-treated rats, their expression was less in all layers. CONCLUSIONSIntravesical instillation with COX-2 inhibitors can reduce CYP-induced bladder hyperactivity and expression of iNOS and NGF. Intravesical instillation with COX-2 inhibitors can be considered as a possible treatment for OAB. KEYWORDSoveractive bladder, inducible nitric oxide synthase, nerve growth factor, cyclooxygenase-2 inhibitors, prostaglandin OBJECTIVETo examine the effects of intravesical cyclooxygenase-2 (COX-2) inhibitors on the expression of inducible nitric oxide synthase (iNOS) and nerve growth factor (NGF) in cyclophosphamide (CYP)-induced overactive bladder (OAB). MATERIALS AND METHODSIn all, 40 Sprague-Dawley rats were divided into control, OAB, and COX-2 inhibitortreated groups. OAB was induced by an intraperitoneal injection with CYP. Cystometry was performed in all rats and, in half of the OAB rats, a COX-2 inhibitor was administered intravesically. The bladders of all rats were

The Association between Chronic Inflammation and Recurrent Cystitis in Women

“…Similar histological findings have been observed in humans with persistent bacteriuria and recurrent UTI [26]. In a rodent model of OAB, Jang et al [27] demonstrated that intravesical cyclooxygenase (COX)-2 inhibitors can alter the expression of inflammatory modulators and cytokines in the bladder tissues improving the parameters of detrusor contraction. In mice, Hannan et al [24] found that the inhibition of COX-2 reduced pyuria and prevented mucosal damage, but did not disrupt any known beneficial mucosal responses, such as urothelial exfoliation and overall immune cell recruitment to the bladder.…”

Biomarkers in the Overactive Bladder Syndrome

“…In the urethra, topical application of PGE 2 causes relaxation of the sphincter (Yokoyama et al, 2007). Likewise, intravesical instillation of an inhibitor of the COX-2 enzyme improved bladder function in an animal model of OAB (Jang et al, 2006). This supports a role for this prostanoid during bladder dysfunction and has justified a few inconclusive clinical trials regarding the use of non-steroidal anti-inflammatory drugs in the treatment of OAB.…”

Effect of hyaluronic acid on urine nerve growth factor in cyclophosphamide‐induced cystitis

“…[17][18][19][20][21][22][23] NGF activity would also increase in cyclophosphamide-induced OAB animal bladder mucosa, submucosa and detrusor. 8 Other clinical investigations had proven the effectiveness of HA on OAB and interstitial cystitis. [24][25][26] The effectiveness of HA treatment in OAB animals can be well shown in the NGF profile of the present study.…”

“…5 Coating the bladder inner surface with other glycoproteins, such as pentosanpolysulphate 6 and hyaluronic acid (HA), is also believed to help prevent further inflammation in the bladder. 7 The increase of bladder hyperactivity 8 and inflammation 9 in cystitis-OAB was found to be related to nerve growth factor (NGF). Increased amounts of NGF in urine has been found in various kinds of pathophysiological bladder conditions, including overactive bladder 10 and inflammatory cystitis.…”