scholarly journals Differentially Expressed Genes Correlated with Fibrosis in a Rat Model of Chronic Partial Bladder Outlet Obstruction

Processes ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 2219
Author(s):  
Yuan-Shuo Hsueh ◽  
Hui-Hua Chang ◽  
Shun-Yao Ko ◽  
Yi-Pai Lin ◽  
Wei-Yu Lin
Keyword(s):  
Differentially Expressed Genes ◽  
Rat Model ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Clinical Problem ◽  
Differentially Expressed ◽  
Partial Bladder Outlet Obstruction ◽  
Bladder Weight ◽  
Gene Expression Alterations ◽  
Tgfb Signaling

Chronic partial bladder outlet obstruction (PBOO) is a prevalent clinical problem that may result from multiple etiologies. PBOO may be a secondary condition to various anatomical and functional abnormalities. Bladder fibrosis is the worst outcome of PBOO. However, gene alterations and the mechanism of fibrosis development after PBOO onset are not clear. Therefore, we aimed to investigate gene expression alterations during chronic PBOO. A rat model of PBOO was established and validated by a significant increase in rat bladder weight. The bladder samples were further analyzed by microarray, and differentially expressed genes (DEGs) that are more related to PBOO compared with the control genes were selected. The data showed that 16 significantly upregulated mRNAs and 3 significantly downregulated mRNAs are involved in fibrosis. Moreover, 13 significantly upregulated mRNAs and 12 significantly downregulated mRNAs are related to TGFB signaling. Twenty-two significantly upregulated mRNAs and nine significantly downregulated mRNAs are related to the extracellular matrix. The genes with differential expressions greater than four-fold included Grem1, Thbs1, Col8a1, Itga5, Tnc, Lox, Timp1, Col4a1, Col4a2, Bhlhe40, Itga1, Tgfb3, and Gadd45b. The gene with a differential expression less than a quarter-fold was Thbs2. These findings show the potential roles of these genes in the physiology of PBOO.

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 Effect of Sulforaphane on Bladder Compliance in a Rat Model of Partial Bladder Outlet Obstruction

2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Chong Liu ◽  
Xiang Wan ◽  
Meng Gu ◽  
Yanbo Chen ◽  
Zhikang Cai ◽  
...  
Keyword(s):  
Rat Model ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Collagen I ◽  
Collagen Deposition ◽  
Sprague Dawley ◽  
Expression Ratio ◽  
Partial Bladder Outlet Obstruction ◽  
Bladder Compliance ◽  
Collagen Iii

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.

EFFECT OF PROLYL 4-HYDROXYLASE INHIBITOR ON THE BLADDER FIBROSIS IN THE RAT MODEL WITH PARTIAL BLADDER OUTLET OBSTRUCTION

2008 ◽  
Vol 179 (4S) ◽  
pp. 221-221
Author(s):  
Jae Min Chung ◽  
Min Jung Jung ◽  
Sang Jin Lee ◽  
Sang Don Lee ◽  
Seong Choi ◽  
...  
Keyword(s):  
Rat Model ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Partial Bladder Outlet Obstruction

scholarly journals Bladder decompensation and reduction in nerve density in a rat model of chronic bladder outlet obstruction are attenuated with the NLRP3 inhibitor glyburide

2019 ◽  
Vol 316 (1) ◽  
pp. F113-F120 ◽  
Author(s):  
Francis M. Hughes ◽  
Stephanie J. Sexton ◽  
Patrick D. Ledig ◽  
Chloe E. Yun ◽  
Huixia Jin ◽  
...  
Keyword(s):  
Rat Model ◽  
Bladder Outlet Obstruction ◽  
Critical Role ◽  
Outlet Obstruction ◽  
Bladder Function ◽  
Postvoid Residual ◽  
Bladder Weight ◽  
Voided Volume ◽  
Postvoid Residual Volume ◽  
Control Sham

Bladder outlet obstruction (BOO) leads to progressive voiding dysfunction. Acutely, obstruction triggers inflammation that drives bladder dysfunction. Over time, inflammation leads to decreased bladder nerve density and increased fibrosis, responsible for eventual decompensation and irreversibility. We have previously shown that BOO triggers inflammation, reduced bladder nerve density and increased fibrosis via activation of the NLRP3 inflammasome in an acutely obstructed (12-day) rat model. However, as BOO progresses, the bladder may become decompensated with an increase in postvoid residual volume and decreased voiding efficiency. Currently, we have examined rat bladder function and nerve densities after chronic BOO to determine whether NLRP3 plays a role in the decompensation at this stage. Four groups were examined: control, sham-operated, BOO, or BOO+gly (glyburide; an NLRP3 inhibitor). After 42 days, bladder weight, inflammation (Evans blue), urodynamics, and nerve density were measured. BOO greatly enhanced bladder weights and inflammation, while inflammation was prevented by glyburide. Voiding pressures were increased, and flow rates decreased in BOO and BOO+gly groups, demonstrating physical obstruction. No difference in frequency or voided volume was detected. However, postvoid residual volumes were greatly increased in BOO rats while BOO+gly rats were not different than controls. Moreover, there was a dramatic decrease in voiding efficiency in the chronic BOO rats, which was prevented with glyburide treatment. Finally, a reduction in nerve density was apparent with BOO and attenuated with glyburide. Together the results suggest a critical role for NLRP3 in mediating bladder decompensation and nerve density during chronic BOO.

Metformin ameliorates bladder dysfunction in a rat model of partial bladder outlet obstruction

2021 ◽  
Vol 320 (5) ◽  
pp. F838-F858
Author(s):  
Lipeng Chen ◽  
Linchen Lv ◽  
Lekai Zhang ◽  
Zhengdong Gao ◽  
Yaxiao Liu ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Rat Model ◽  
Bladder Outlet Obstruction ◽  
Bladder Dysfunction ◽  
Outlet Obstruction ◽  
Term Treatment ◽  
Potential Drug ◽  
Partial Bladder Outlet Obstruction ◽  
Long Term Treatment

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.

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