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 ◽  
...  

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.

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Chong Liu ◽  
Huan Xu ◽  
Shi Fu ◽  
Yanbo Chen ◽  
Qi Chen ◽  
...  

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.


Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1285
Author(s):  
Nozomu Miyazaki ◽  
Ryota Katsura ◽  
Koki Hamada ◽  
Tatsuo Suzutani

Various berries demonstrate antioxidant activity, and this effect is expected to prevent chronic diseases. We examined whether a diet containing blueberry powder could prevent the development of bladder dysfunction secondary to bladder outlet obstruction (BOO). Eighteen 8-week-old male Sprague-Dawley rats were randomly divided into three groups: Sham (sham operated + normal diet), N-BOO (BOO operated + normal diet) and B-BOO (BOO operated + blueberry diet). Four weeks after BOO surgery, the N-BOO group developed bladder dysfunction with detrusor overactivity. The B-BOO group showed significantly improved micturition volume and micturition interval. The urinary levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG) and malondialdehyde (MDA) were measured as oxidative stress markers. In the N-BOO group, 8-OHdG increased 1.6-fold and MDA increased 1.3-fold at 4 weeks after surgery, whereas the increase in 8-OHdG was significantly reduced by 1.1-fold, despite a similar increase in MDA, in the B-BOO group. Bladder remodeling was confirmed due to bladder hypertrophy, fibrosis and increased connexin43 expression in the N-BOO group, but these histological changes were reduced in the B-BOO group. The intake of blueberries prevented the development of bladder dysfunction secondary to BOO. This effect seems to be related to antioxidation and the inhibition of bladder remodeling.


2018 ◽  
Author(s):  
Min Soo Choo ◽  
SongZhe Piao ◽  
Seung-June Oh

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.


2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Chong Liu ◽  
Xiang Wan ◽  
Meng Gu ◽  
Yanbo Chen ◽  
Zhikang Cai ◽  
...  

Aims. To investigate the effect of Nrf2 activator sulforaphane (SFN) on bladder compliance and the underlying mechanisms in a rat model of partial bladder outlet obstruction (BOO). Methods. Male 8-week-old Sprague-Dawley rats were divided into three groups. BOO rats were given daily 0.5 mg/kg sulforaphane (BOO+SFN) or vehicle (BOO) intraperitoneally for 4 weeks, while sham-operated rats were treated with vehicle (Sham). Bladder compliance, histological alteration, and collagen deposition were evaluated. The expression levels of collagen I, collagen III, MMP-1, and TIMP-1 were measured by immunohistochemistry and western blotting. Results. BOO led to a significant decrease in bladder compliance. The change was partially restored by SFN treatment. The expression of MMP-1 was significantly decreased accompanying with increased TIMP-1 expression in BOO rats compared with that in Sham rats, which was ameliorated by SFN treatment. Moreover, the increased collagen I/collagen III ratio in the BOO group was reversed by SFN treatment. Conclusions. Sulforaphane suppressed collagen deposition by regulating the MMP-1 and TIMP-1 expression and decreasing the collagen I/III expression ratio in BOO rats and improved bladder compliance.


2021 ◽  
Vol 320 (5) ◽  
pp. F838-F858
Author(s):  
Lipeng Chen ◽  
Linchen Lv ◽  
Lekai Zhang ◽  
Zhengdong Gao ◽  
Yaxiao Liu ◽  
...  

The present study in a rat model showed that oral administration of metformin alleviated inflammation following partial bladder outlet obstruction in the early phase and ameliorated bladder fibrosis as well as bladder dysfunction by long-term treatment. Our study indicated that metformin is a potential drug to inhibit bladder remodeling and alleviate bladder dysfunction. Clinical trials are needed to validate the effect of metformin on the bladder dysfunction and bladder fibrosis in the future.


2009 ◽  
Vol 182 (1) ◽  
pp. 382-390 ◽  
Author(s):  
Michiko Oka ◽  
Tomomi Fukui ◽  
Makoto Ueda ◽  
Mitsuhiro Tagaya ◽  
Tatsuya Oyama ◽  
...  

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