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

机译:萝卜硫素通过激活部分膀胱出口梗阻大鼠模型中的Nrf2-ARE途径改善膀胱功能障碍。

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摘要

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.
机译:目的。我们评估了萝卜硫烷(SFN)对膀胱出口梗阻(BOO)大鼠膀胱功能和Nrf2-ARE途径表达的影响。材料和方法。将总共​​18只8周大的雄性Sprague-Dawley大鼠分为3组(每组6只):假手术组,BOO组和BOO + SFN组。我们检查了组织学变化,氧化应激标志物的变化和Nrf2-ARE途径的蛋白质表达。结果。我们发现,SFN治疗可延长排尿间隔并增加膀胱容量和膀胱顺应性。但是,峰值排尿压力低于BOO组。 SFN治疗可以改善阻塞引起的胶原纤维的增加。与其他组相比,SFN处理还增加了SOD,GSH-Px和CAT的活性。 SFN处理的BOO大鼠膀胱细胞凋亡水平降低。而且,SFN可以降低Bax / Bcl-2表达的比率。此外,SFN可以通过提高其目标抗氧化剂蛋白来激活Nrf2表达。结论。萝卜硫烷介导的氧化应激降低和Nrf2-ARE途径的激活可能会减轻由膀胱出口梗阻引起的膀胱功能障碍。

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