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在部分膀胱出口梗阻大鼠模型中,萝卜硫素通过激活Nrf2-ARE通路改善膀胱功能障碍。

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

作者信息

Liu Chong, Xu Huan, Fu Shi, Chen Yanbo, Chen Qi, Cai Zhikang, Zhou Juan, Wang Zhong

机构信息

Department of Urology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.

出版信息

Oxid Med Cell Longev. 2016;2016:7598294. doi: 10.1155/2016/7598294. Epub 2016 Jun 28.

DOI:10.1155/2016/7598294
PMID:27433291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4940551/
Abstract

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.

摘要

目的。我们评估了萝卜硫素(SFN)治疗对膀胱出口梗阻(BOO)大鼠膀胱中Nrf2-ARE通路功能及表达变化的影响。材料与方法。将18只8周龄雄性Sprague-Dawley大鼠分为3组(每组6只):假手术组、BOO组和BOO+SFN组。我们检查了组织学改变、氧化应激标志物变化以及Nrf2-ARE通路的蛋白表达。结果。我们发现SFN治疗可延长排尿间隔、增加膀胱容量和膀胱顺应性。然而,最大排尿压力低于BOO组。SFN治疗可改善梗阻诱导的胶原纤维增加。与其他组相比,SFN治疗还增加了超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)的活性。SFN治疗的BOO大鼠膀胱细胞凋亡水平降低。此外,SFN可降低Bax/Bcl-2表达比值。此外,SFN可通过提高其靶标抗氧化蛋白的水平来激活Nrf2表达。结论。萝卜硫素介导的氧化应激降低和Nrf2-ARE通路激活可能改善膀胱出口梗阻引起的膀胱功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/40add42620c1/OMCL2016-7598294.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/ace2226e3aa2/OMCL2016-7598294.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/d3db965c0ed8/OMCL2016-7598294.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/1217e2a49072/OMCL2016-7598294.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/cd80ee29d8c7/OMCL2016-7598294.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/40add42620c1/OMCL2016-7598294.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/ace2226e3aa2/OMCL2016-7598294.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/d3db965c0ed8/OMCL2016-7598294.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/1217e2a49072/OMCL2016-7598294.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/cd80ee29d8c7/OMCL2016-7598294.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abfe/4940551/40add42620c1/OMCL2016-7598294.005.jpg

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