Suppression of Bladder Oxidative Stress and Inflammation by a Phytotherapeutic Agent in a Rat Model of Partial Bladder Outlet Obstruction

Oka, Michiko; Fukui, Tomijiro; Ueda, Makoto; Tagaya, Mitsuhiro; Oyama, Tatsuya; Tanaka, Mitsushi

doi:10.1016/j.juro.2009.02.104

Cited by 63 publications

(100 citation statements)

References 14 publications

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“…The changes in the bladder weight after pBOO were consistent with the changes seen in previous studies (2, 3, 21,22,30). pBOO clearly induced time-dependent increases in bladder weight that continued until day 7; these increases seemed to reach a plateau by day 14 after pBOO.…”

Section: Discussionsupporting

confidence: 90%

Increased expression of 5-HT2A and 5-HT2B receptors in detrusor muscle after partial bladder outlet obstruction in rats

et al. 2015

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Serotonin (5-hydroxytryptamine; 5-HT)-induced bladder contraction is enhanced after partial bladder outlet obstruction (pBOO) in rats. We investigated time-dependent changes in bladder contraction and expression of 5-HT 2A and 5-HT 2B receptor mRNA in bladder tissue to elucidate the mechanism of this enhancement. On day 3 and 7 after pBOO, contractile responses of isolated rat bladder strips to 5-HT were increased compared with that in sham-operated rats; on day 14, the response had decreased to the same level as that in sham rat bladders. In contrast, carbacholinduced contraction was not enhanced by pBOO at any time point. In sham rats, 5-HT 2A receptor mRNA was expressed in the urothelium, and 5-HT 2B receptor mRNA was expressed in the detrusor muscle layer. In pBOO rats, both receptor mRNAs were increased in the detrusor muscle and subserosal layers, but not in the urothelium. The increase of 5-HT 2A receptor mRNA was maintained from day 3 to day 14 after pBOO, and 5-HT 2B receptor mRNA was increased on day 7 after pBOO. These results suggested that pBOO induced up-regulation of the 5-HT 2A and 5-HT 2B receptors in the detrusor muscle and subserosal layers of the bladder, and such up-regulation may be related to the enhanced bladder contractile response to 5-HT.Partial bladder outlet obstruction (pBOO) secondary to benign prostate hyperplasia has been considered an important factor associated with lower urinary tract symptoms (LUTS). LUTS include voiding symptoms (e.g., weak urine stream and urinary retention) and storage symptoms (e.g., urinary frequency, urgency and nocturia) (1). Voiding symptom is attributed to increased urethral resistance due to static and dynamic prostatic obstruction. In contrast, the mechanism responsible for storage symptoms secondary to pBOO remains unknown. To clarify the mechanism, several changes in the bladder have been investigated with animal models of pBOO (13,14,17). In these animal models, urothelium, subserosal layer, and detrusor muscle layer of the bladder are thickened (2, 7, 24). These morphological alterations result in some functional changes, such as detrusor overactivity. These morphological and functional alterations reach different states at different time points after pBOO (2,16,19). Therefore, both morphological and functional changes must be evaluated at several time points to reveal the mechanisms responsible for the storage symptoms secondary to pBOO. One of the important functional changes in the bladder with pBOO is the contractile response associated with detrusor overactivity. Contractile responses to ATP and acetylcholine are changed by pBOO; however, descriptions of these changes are not consistent among reports (2,7,19,25). Therefore, the myogenic change caused by pBOO is not fully understood. Serotonin (5-hydroxytryptamine; 5-HT) is a mono-

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Section: Discussionsupporting

confidence: 90%

Increased expression of 5-HT2A and 5-HT2B receptors in detrusor muscle after partial bladder outlet obstruction in rats

et al. 2015

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“…But, Shabsigh et al reported castration resulted in a rapid and significant reduction of blood flow to the rat ventral prostate gland that was not seen in the bladder [11]. In this results, bladder contractile forces in response to EFS (2,8, and 32 Hz), carbachol and KCl did not change in NBP rats. These results indicated the bladder function is not influenced in this NBP model.…”

Section: Discussionmentioning

confidence: 50%

“…Contractile responses were measured as described by Oka et al [8]. The bladder dome was removed and full-thickness longitudinal strips of about 3 × 10 mm were taken from the bladder body.…”

Section: Contractility Measurements In Isolated Bladder Smooth-musclementioning

confidence: 99%

Bladder function in 17β-estradiol-induced nonbacterial prostatitis model in Wister rat

et al. 2013

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Objectives: To investigated the bladder function of nonbacterial prostatitis (NBP) rat model that was induced by the injection of 17-estradiol in castrated rats. Methods:Ten-month-old male Wistar rats were divided into 2 groups (sham vs NBP; each N=8). NBP model was experimentally induced by castration followed by daily subcutaneous injection of 17-estradiol for 30 days. On the 31st day after surgery, we investigated several parameters; (1) Voiding behavior, (2) Bladder blood flow, (3) Measurements of the prostate and bladder weight, the levels of proinflammatory cytokines (TNF- and CXCL1) in the prostate and bladder, (4) Bladder contractile responses to electrical field stimulation (EFS), carbachol, and KCl.Results: (1) Voiding behavior (average micturition volume, total urine volume and number of micturitions) and (2) bladder blood flow were not significantly different between sham and NBP group. (3) NBP led to a significant decrease in the prostatic weight and increase in proinflammatory cytokine levels in the prostate, while NBP did not cause a significant change in the bladder weight or proinflammatory cytokine levels in the bladder.(4) Bladder contractile forces in response to EFS, carbachol and KCl were not significantly different between sham and NBP group. Conclusions:The present study suggests that NBP did not cause a significant change in the levels of proinflammatory cytokines in the bladder, and the bladder function is not influenced in this NBP model. Matsumoto S, et al. Bladder function in rat NBP model -3 -

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“…The histological examination of the BOO rat bladder showed that there was infiltration of inflammatory cells in the bladder, including mast cells. BOO causes ischemic reperfusion and oxidative stress within the bladder, which can then induce bladder inflammation (26,35). Previous studies have demonstrated that ischemia and inflammation cause platelet activation and the release of 5-HT (34,37).…”

Section: Discussionmentioning

confidence: 99%

5-Hydroxytryptamine-induced bladder hyperactivity via the 5-HT_2Areceptor in partial bladder outlet obstruction in rats

Sakai

Kasahara

Tomita

et al. 2013

American Journal of Physiology-Renal Physiology

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We investigated the effects of partial bladder outlet obstruction (BOO) on the function and gene expression of 5-hydroxytryptamine (5-HT) receptor subtypes in rat bladder. Isometric contractions of the isolated bladders from sham-operated control and BOO rats were examined. The contractile responses to 5-HT were significantly increased in BOO rat bladder strips, while the responses to KCl, carbachol, or phenylephrine were not different from the control. The 5-HT-induced hypercontraction in BOO rat bladder strips was inhibited by ketanserin, a 5-HT(2A) receptor antagonist. The contractile responses to 5-HT in bladder strips were not affected by urothelium removal from the intact bladder. The gene expression of 5-HT receptor subtypes in the bladders was analyzed by RT-PCR. The mRNA expression of the 5-HT(2A), 5-HT(2B), 5-HT(2C), 5-HT(4), and 5-HT(7) receptors was detected in both the control and BOO rat bladders. Quantitative RT-PCR analysis showed there was a significant increase of 5-HT(2A) receptor mRNA in the BOO rat bladder compared with the control bladder. On the other hand, the gene expression of the 5-HT(4) receptor was not changed in the BOO rat bladder. These results suggest that the increased contractile responses to 5-HT in BOO rat bladder may be partly caused by 5-HT(2A) receptor upregulation in the detrusor smooth muscles.

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Suppression of Bladder Oxidative Stress and Inflammation by a Phytotherapeutic Agent in a Rat Model of Partial Bladder Outlet Obstruction

Abstract: Eviprostat mediated decrease of the increased oxidative stress and bladder inflammation caused by bladder outlet obstruction may contribute to the protection of bladder function.

Cited by 63 publications

References 14 publications

<b>Increased expression of 5-HT</b><b><sub>2A</sub></b><b> and 5-HT</b><b><sub>2B</sub></b><b> receptors in detrusor muscle after partial bladder outlet obstruction in </b><b>rats </b>

<b>Increased expression of 5-HT</b><b><sub>2A</sub></b><b> and 5-HT</b><b><sub>2B</sub></b><b> receptors in detrusor muscle after partial bladder outlet obstruction in </b><b>rats </b>

Bladder function in 17β-estradiol-induced nonbacterial prostatitis model in Wister rat

5-Hydroxytryptamine-induced bladder hyperactivity via the 5-HT_2Areceptor in partial bladder outlet obstruction in rats

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Suppression of Bladder Oxidative Stress and Inflammation by a Phytotherapeutic Agent in a Rat Model of Partial Bladder Outlet Obstruction

Abstract: Eviprostat mediated decrease of the increased oxidative stress and bladder inflammation caused by bladder outlet obstruction may contribute to the protection of bladder function.

Cited by 63 publications

References 14 publications

<b>Increased expression of 5-HT</b><b><sub>2A</sub></b><b> and 5-HT</b><b><sub>2B</sub></b><b> receptors in detrusor muscle after partial bladder outlet obstruction in </b><b>rats </b>

<b>Increased expression of 5-HT</b><b><sub>2A</sub></b><b> and 5-HT</b><b><sub>2B</sub></b><b> receptors in detrusor muscle after partial bladder outlet obstruction in </b><b>rats </b>

Bladder function in 17β-estradiol-induced nonbacterial prostatitis model in Wister rat

5-Hydroxytryptamine-induced bladder hyperactivity via the 5-HT2Areceptor in partial bladder outlet obstruction in rats

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5-Hydroxytryptamine-induced bladder hyperactivity via the 5-HT_2Areceptor in partial bladder outlet obstruction in rats