scholarly journals A Review of Oxidative Stress and Urinary Dysfunction Caused by Bladder Outlet Obstruction and Treatments Using Antioxidants

Antioxidants ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 132 ◽  
Author(s):  
Yasuyoshi Miyata ◽  
Tomohiro Matsuo ◽  
Kensuke Mitsunari ◽  
Akihiro Asai ◽  
Kojiro Ohba ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bladder Outlet Obstruction ◽  
Pathological Condition ◽  
Ischemia Reperfusion ◽  
Animal Experiments ◽  
Treatment Strategies ◽  
Outlet Obstruction ◽  
Urinary Dysfunction ◽  
Research Issues ◽  
Stress Changes

Urinary dysfunction is a common pathological condition that can significantly decrease the quality of life. Bladder outlet obstruction (BOO) is a major cause of urinary dysfunction, and various lower urinary tract diseases including benign prostatic hyperplasia and urethral stricture disease cause BOO. According to the results of a variety of animal experiments on partial BOO (PBOO), there is a general agreement that ischemic conditions and repeated ischemia/reperfusion of the bladder are closely associated with BOO-induced bladder damage, and that increased oxidative stress by ischemia/reperfusion plays a crucial role in the pathological mechanisms underlying urinary dysfunction. Changes in biomarkers of oxidative stress in PBOO animal models support this association between oxidative stress and urinary dysfunction. Oxidative stress is defined as an imbalance between the production of pro-oxidants, such as free radicals and reactive species, and their elimination through protective mechanisms of antioxidants. Therefore, organizing the knowledge on the state of oxidative stress, changes in biomarkers, and biological roles of antioxidants in systemic and bladder tissues is essential to understand the detailed pathological characteristics of the urinary dysfunction caused by PBOO. Furthermore, information on drugs and supplements that have antioxidant effects is important for defining treatment strategies for urinary dysfunction with PBOO. In this review, we paid special attention to the following three issues; (1) changes in oxidative stress, including its biomarkers, (2) antioxidant status, and (3) previous reports on treatment strategies involving agents with antioxidative activity for urinary dysfunction caused by BOO. In particular, we provide systematic information on the detailed mechanisms underlying the antioxidative effects of agents used to treat PBOO. In addition, we show present research issues and research limitations, as well as suggest possible future antioxidant treatment strategies for patients with PBOO.

scholarly journals Bladder Hyperactivity Induced by Oxidative Stress and Bladder Ischemia: A Review of Treatment Strategies with Antioxidants

2021 ◽  
Vol 22 (11) ◽  
pp. 6014
Author(s):  
Yi-Hsuan Wu ◽  
Kuang-Shun Chueh ◽  
Shu-Mien Chuang ◽  
Cheng-Yu Long ◽  
Jian-He Lu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Negative Impact ◽  
Ischemia Reperfusion ◽  
Treatment Strategies ◽  
Outlet Obstruction ◽  
Urinary Dysfunction ◽  
Hormone Deficiency ◽  
Bladder Tissue ◽  
Quality Of Life Scale ◽  
Bladder Ischemia

Overactive bladder (OAB) syndrome, including frequency, urgency, nocturia and urgency incontinence, has a significantly negative impact on the quality-of-life scale (QoL) and can cause sufferer withdrawal from social activities. The occurrence of OAB can result from an imbalance between the production of pro-oxidants, such as free radicals and reactive species, and their elimination through protective mechanisms of antioxidant-induced oxidative stress. Several animal models, such as bladder ischemia/reperfusion (I/R), partial bladder outlet obstruction (PBOO) and ovarian hormone deficiency (OHD), have suggested that cyclic I/R during the micturition cycle induces oxidative stress, leading to bladder denervation, bladder afferent pathway sensitization and overexpression of bladder-damaging molecules, and finally resulting in bladder hyperactivity. Based on the results of previous animal experiments, the present review specifically focuses on four issues: (1) oxidative stress and antioxidant defense system; (2) oxidative stress in OAB and biomarkers of OAB; (3) OAB animal model; (4) potential nature/plant antioxidant treatment strategies for urinary dysfunction with OAB. Moreover, we organized the relationships between urinary dysfunction and oxidative stress biomarkers in urine, blood and bladder tissue. Reviewed information also revealed the summary of research findings for the effects of various antioxidants for treatment strategies for OAB.

scholarly journals A corticotropin-releasing factor receptor antagonist improves urodynamic dysfunction produced by social stress or partial bladder outlet obstruction in male rats

2013 ◽  
Vol 304 (11) ◽  
pp. R940-R950 ◽  
Author(s):  
Susan K. Wood ◽  
Kile McFadden ◽  
Tagan Griffin ◽  
John H. Wolfe ◽  
Stephen Zderic ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Social Stress ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Bladder Capacity ◽  
Urinary Dysfunction ◽  
Male Rats ◽  
Inhibitory Influence ◽  
Partial Bladder Outlet Obstruction ◽  
Final Stress

Barrington's nucleus, in the pons, regulates micturition through spinal projections to preganglionic parasympathetic neurons. The stress neuropeptide CRF is prominent in these projections and has an inhibitory influence. Social stress in rats causes urinary retention and abnormal urodynamics resembling those produced by partial bladder outlet obstruction (pBOO), and this is associated with CRF upregulation in Barrington's nucleus. Here, we examined the role of CRF in social stress- and pBOO-induced urodynamic dysfunction by assessing the ability of a CRF1 receptor antagonist to alter these effects. Male rats exposed to repeated resident-intruder stress were administered vehicle or a CRF1 antagonist (NBI-30775) daily prior to the stress. Urodynamic function was recorded in the unanesthetized state 72 h after the final stress. NBI-30775 prevented the increased intermicturition interval, micturition volume, and bladder capacity produced by social stress, but not the increase in CRF expression in Barrington's nucleus neurons. The urinary dysfunction was also partly prevented by shRNA targeting of CRF in Barrington's nucleus, suggesting that stress-induced urinary dysfunction results, in part, from CRF upregulation in Barrington's nucleus and enhanced postsynaptic effects in the spinal cord. Finally, NBI-30775 improved urodynamic function of rats that had pBOO of 2-wk duration when administered daily during the second week but did not block the increase in CRF expression in Barrington's nucleus neurons. These findings implicate a role for Barrington's nucleus CRF in stress- and pBOO-induced urodynamic changes and suggest that CRF1 antagonists may be useful therapeutic agents for the treatment of urinary dysfunction.

Reversing bladder outlet obstruction attenuates systemic and tissue oxidative stress

2012 ◽  
Vol 110 (8) ◽  
pp. 1208-1213 ◽  
Author(s):  
Wei-Yu Lin ◽  
Shi-Bei Wu ◽  
Yi-Pai Lin ◽  
Pey-Jium Chang ◽  
Robert M. Levin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction

scholarly journals The effect of a free radical scavenger on oxidation stress in partial bladder outlet obstruction and its relief in a rat model

2018 ◽  
Author(s):  
Min Soo Choo ◽  
SongZhe Piao ◽  
Seung-June Oh
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Rat Model ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Detrusor Muscle ◽  
Oxidation Stress ◽  
Partial Bladder Outlet Obstruction

AbstractAIMSTo investigate the effect of a free radical scavenger (tempol) after relief of partial bladder outlet obstruction (pBOO) on bladder function in a rat model.METHODSpBOO was induced in 50 eight-week-old female Sprague-Dawley rats and relieved 3 weeks later. The rats were divided randomly into 5 groups: sham-operated, tempol-treated for 1 week (Treat-1w) or 3 weeks (Treat-3w), and no treatment for 1 week (nonTreat-1w) or 3 weeks (nonTreat-3w). Awaken cystometrograms were obtained 1 or 3 weeks after relief according to the grouping. The bladders were isolated and weighed. H&E, Masson’s trichrome and TUNEL staining were used to analyze histological changes. The oxidative stress assessed using malondialdehyde. The expression of beta-3 adrenoreceptor was examined by Western blotting.RESULTSThe tempol-treated groups exhibited a significant decrease in the number of IDCs per voiding cycle (nonTreat-1w vs. Treat-1w, 1.18±0.82 vs. 0.36±0.40, P=0.010; nonTreat-3w vs. Treat-3w, 1.51±0.69 vs. 0.23±0.25, P=0.002). The thickness and collagen fiber deposition of the detrusor muscle layer was significantly decreased in the treated groups. Apoptosis detected was mainly observed in the urothelial cell layer, although the rate of apoptosis was significantly decreased in the treated groups (48.9±3.36% vs. 32.7±11.10%, P=0.024; 25.8±4.67% vs. 15.7±9.83%, P=0.314). The tempol-treated groups showed significant decreases in the MDA concentrations at both 1 and 3 weeks after relief. The expression of the beta-3 adrenoreceptor was increased in the tempol-treated rats.CONCLUSIONSIschemic reperfusion injury after relief of pBOO caused histological and functional changes in the bladder. Free radical scavenger treatment prevented this oxidative stress.

scholarly journals Epigallocatechin Gallate Attenuates Bladder Dysfunction via Suppression of Oxidative Stress in a Rat Model of Partial Bladder Outlet Obstruction

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Meng Gu ◽  
Chong Liu ◽  
Xiang Wan ◽  
Tianye Yang ◽  
Yanbo Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Rat Model ◽  
Bladder Outlet Obstruction ◽  
Bladder Dysfunction ◽  
Outlet Obstruction ◽  
Epigallocatechin Gallate ◽  
Saline Control ◽  
Tunel Staining ◽  
Sprague Dawley

Purpose. To investigate the protective effect of epigallocatechin gallate (EGCG), a green tea extract, and its underlying mechanism on bladder dysfunction in a rat model of bladder outlet obstruction (BOO). Materials and Methods. Sprague-Dawley rats of BOO were surgically induced and followed by treatment with EGCG (5 mg/kg/day) or saline (control) via intraperitoneal injection. Cystometry was performed on four weeks postoperatively in conscious rats. H&E, Masson trichrome, and TUNEL staining were performed to observe tissue alterations. Oxidative stress markers were measured, and protein expression of Nrf2-ARE pathway was examined by immunohistochemistry and Western blotting. Results. Our data showed that EGCG could increase the peak voiding pressure and bladder compliance and prolong micturition interval of BOO rats compared with control and finally reduce the frequency of urinary. EGCG could ameliorate the increase of collagen fibers and ROS induced by obstruction and increase the activity of SOD, GSH-Px, and CAT. The level of cell apoptosis was decreased in BOO rats treated with EGCG compared with control, and caspase-3 expression was reduced as well. Moreover, EGCG could activate the Nrf2 expression with elevation of its target antioxidant proteins. Conclusions. EGCG alleviates BOO-induced bladder dysfunction via suppression of oxidative stress and activation of the protein expression of Nrf2-ARE pathway.

scholarly journals Sulforaphane Ameliorates Bladder Dysfunction through Activation of the Nrf2-ARE Pathway in a Rat Model of Partial Bladder Outlet Obstruction

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Chong Liu ◽  
Huan Xu ◽  
Shi Fu ◽  
Yanbo Chen ◽  
Qi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bladder Outlet Obstruction ◽  
Bladder Dysfunction ◽  
Outlet Obstruction ◽  
Bladder Capacity ◽  
Sprague Dawley ◽  
Stress Markers ◽  
Bladder Cell ◽  
Sprague Dawley Rats ◽  
Antioxidant Proteins

Purpose. We evaluated the effect of sulforaphane (SFN) treatment on the function and changes of expression of Nrf2-ARE pathway in the bladder of rats with bladder outlet obstruction (BOO).Materials and Methods. A total of 18 male Sprague-Dawley rats at age of 8 weeks were divided into 3 groups (6 of each): the sham operated group, the BOO group, and the BOO+SFN group. We examined histological alterations and the changes of oxidative stress markers and the protein expression of the Nrf2-ARE pathway.Results. We found that SFN treatment could prolong micturition interval and increase bladder capacity and bladder compliance. However, the peak voiding pressure was lower than BOO group. SFN treatment can ameliorate the increase of collagen fibers induced by obstruction. SFN treatment also increased the activity of SOD, GSH-Px, and CAT compared to the other groups. The level of bladder cell apoptosis was decreased in BOO rats with SFN treatment. Moreover, SFN could reduce the ratio of Bax/Bcl-2 expression. Furthermore, SFN could activate the Nrf2 expression with elevation of its target antioxidant proteins.Conclusions. The sulforaphane-mediated decrease of oxidative stress and activation of the Nrf2-ARE pathway may ameliorate bladder dysfunction caused by bladder outlet obstruction.

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

2009 ◽  
Vol 182 (1) ◽  
pp. 382-390 ◽  
Author(s):  
Michiko Oka ◽  
Tomomi Fukui ◽  
Makoto Ueda ◽  
Mitsuhiro Tagaya ◽  
Tatsuya Oyama ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Partial Bladder Outlet Obstruction
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