Protective effect of <i>N</i>‐acetylcysteine against ischemia/reperfusion injury in rat urinary bladders

Shin, Ju Hyun; Kim, Gun-Hwa; Song, Kyu‐Sang; Na, Yong Gil; Sul, Chong Koo; Lim, Jaesung

doi:10.1002/cbf.2967

Cited by 7 publications

(8 citation statements)

References 40 publications

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“…Overactive bladder (OAB) is prevalent in patients or animal models with diabetes [ 12 ], bladder outlet obstruction [ 13 ], chronic ischemia [ 14 ], ischemia/reperfusion [ 15 ], or ageing [ 16 ]. These pathophysiological conditions are also characterized by excessive accumulation of reactive oxygen species (ROS).…”

Section: Introductionmentioning

confidence: 99%

Regulation of Spontaneous Contractions in Intact Rat Bladder Strips and the Effects of Hydrogen Peroxide

Wang

Xing

et al. 2018

BioMed Research International

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Enhanced spontaneous contractions are associated with overactive bladder. Elevated levels of reactive oxygen species might contribute to enhanced spontaneous contractions. We investigated the regulation of spontaneous contractions and the effects of hydrogen peroxide (H2O2) in intact rat bladder strips. The spontaneous contractions were measured using a tissue bath system. The vehicle or the specific activators/blockers were applied and followed by the application of 0.003 g% H2O2. The basal tension, amplitude, and frequency of spontaneous contractions were quantified. Nisoldipine and bisindolylmaleimide 1 had no effects on spontaneous contractions. SKF96365 and Y27632 decreased basal tension and amplitude. Ryanodine slightly increased frequency. Both iberiotoxin and NS-1619 increased amplitude. Apamin reduced frequency but increased amplitude. NS-309 inhibited both the amplitude and frequency. The basal tension and amplitude increased when H2O2 was applied. Pretreatment with NS-309 inhibited H2O2-elicited augmented amplitude and frequency, while pretreatment with Y-27632 inhibited the augmented basal tension. The combined application of NS-309 and Y27632 almost eliminated spontaneous contractions and its augmentation induced by H2O2. In conclusion, Ca2+ influx, Rho kinase activation, and SK channel inactivation play important roles in spontaneous contractions in intact bladder strips, whereas only latter two mechanisms may be involved in H2O2-elicited increased spontaneous contractions.

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Section: Introductionmentioning

confidence: 99%

Regulation of Spontaneous Contractions in Intact Rat Bladder Strips and the Effects of Hydrogen Peroxide

Wang

Xing

et al. 2018

BioMed Research International

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“…Recently, we showed that bladder I/R injury leads to the formation of lipid peroxidation [ 14 ]. Considering these results, the above finding, which indicated that allopurinol had antioxidant effects, prompted us to determine whether allopurinol treatments can also regulate the levels of lipid peroxidation.…”

Section: Resultsmentioning

confidence: 99%

“…MDA amounts were assayed with a thiobarbituric acid reactive substances (TBARS) kit (ZeptoMetrix), which is based on a spectroscopic method. MDA levels were performed according to standard protocol as previously described [ 14 ].…”

Section: Methodsmentioning

confidence: 99%

Allopurinol Protects against Ischemia/Reperfusion-Induced Injury in Rat Urinary Bladders

Shin

Chun

et al. 2015

Oxidative Medicine and Cellular Longevity

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Bladder ischemia-reperfusion (I/R) injury results in the generation of reactive oxygen species (ROS) and markedly elevates the risk of lower urinary tract symptoms (LUTS). Allopurinol is an inhibitor of xanthine oxidase (XO) and thus can serve as an antioxidant that reduces oxidative stress. Here, a rat model was used to assess the ability of allopurinol treatment to ameliorate the deleterious effects of urinary bladder I/R injury. I/R injury reduced the in vitro contractile responses of longitudinal bladder strips, elevated XO activity in the plasma and bladder tissue, increased the bladder levels of tumor necrosis factor-α (TNF-α), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase, reduced the bladder levels of extracellular regulated kinase (ERK), and decreased and increased the bladder levels of Bcl-2 and Bax, respectively. I/R injury also elevated lipid peroxidation in the bladder. Allopurinol treatment in the I/R injury was generated significantly ameliorating all I/R-induced changes. Moreover, an in situ fluorohistological approach also showed that allopurinol reduces the generation of intracellular superoxides enlarged by I/R injury. Together, the beneficial effects of allopurinol reducing ROS production may be mediated by normalizing the activity of the ERK, JNK, and Bax/Bcl-2 pathways and by controlling TNF-α expression.

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“…Several other agents possessing such properties have been shown to have protective effects against ischemia-reperfusion bladder injuries, for example, co-enzyme Q [Juan et al 2008; Kim et al 2013], N-acetylcysteine [Shin et al 2014], eviprostat [Matsui et al 2012; Kawai et al 2013] and edaravone [Matsumoto et al 2010]. Some of these agents may also be useful for protection against the effects of chronic bladder ischemia.…”

Section: Free Radical Scavengingmentioning

confidence: 99%

Pharmacological treatment of chronic pelvic ischemia

Andersson

Nomiya

Sawada

et al. 2014

Therapeutic Advances in Urology

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Abstract:Epidemiological studies have shown that lower urinary tract symptoms, including overactive bladder, commonly occur in both men and women, with an age-related increase in both sexes. Vascular endothelial dysfunction and urological symptoms are common in the metabolic syndrome; they also occur during the human ageing process and are independent risk factors for the development of atherosclerosis and hypertension. Pelvic arterial insufficiency may lead to impaired lower urinary tract perfusion and play an important role in the development of bladder dysfunction such as detrusor overactivity and overactive bladder. It seems reasonable, but has not been definitely established clinically, that chronic ischemiarelated bladder dysfunction will progress to bladder underactivity. Studies in experimental models in rabbits and rats have shown that pelvic arterial insufficiency may result in significant bladder ischemia with reduced bladder wall oxygen tension, oxidative stress, increased muscarinic receptor activity, ultrastructural damage, and neurodegeneration. Several types of drug may be able to prevent some of these changes. Even if the α 1 -adrenoceptor blocker, silodosin, the phosphodiesterase type 5 inhibitor, tadalafil, the β 3 -α 1 -adrenoceptor agonist, mirabegron, and the free radical scavenger, melatonin, were unable to prevent the development of neointimal hyperplasia and consequent luminal occlusion in animal models, they all exerted a protecting effect on urodynamic parameters, and on the functional and morphological changes of the bladder demonstrable in vitro. The different mechanisms of action of the drugs suggest that many factors are involved in the pathogenesis of chronic ischemia-induced bladder dysfunction and can be targets for intervention. Since several of the agents tested are used clinically and effectively for relieving lower urinary tract symptoms, the results from animal models of chronic bladder ischemia seem to have translational value. Animal models may be of relevance for designing clinical studies to demonstrate if a certain drug may prevent progression of ischemia-related functional and morphological bladder changes.

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Protective effect of N‐acetylcysteine against ischemia/reperfusion injury in rat urinary bladders

Cited by 7 publications

References 40 publications

Regulation of Spontaneous Contractions in Intact Rat Bladder Strips and the Effects of Hydrogen Peroxide

Regulation of Spontaneous Contractions in Intact Rat Bladder Strips and the Effects of Hydrogen Peroxide

Allopurinol Protects against Ischemia/Reperfusion-Induced Injury in Rat Urinary Bladders

Pharmacological treatment of chronic pelvic ischemia

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