scholarly journals Blueberry Prevents the Bladder Dysfunction in Bladder Outlet Obstruction Rats by Attenuating Oxidative Stress and Suppressing Bladder Remodeling

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1285
Author(s):  
Nozomu Miyazaki ◽  
Ryota Katsura ◽  
Koki Hamada ◽  
Tatsuo Suzutani
Keyword(s):  
Oxidative Stress ◽  
Bladder Outlet Obstruction ◽  
Bladder Dysfunction ◽  
Outlet Obstruction ◽  
Normal Diet ◽  
Sprague Dawley ◽  
Histological Changes ◽  
Stress Markers ◽  
Sprague Dawley Rats ◽  
Micturition Volume

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.

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

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Chong Liu ◽  
Huan Xu ◽  
Shi Fu ◽  
Yanbo Chen ◽  
Qi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bladder Outlet Obstruction ◽  
Bladder Dysfunction ◽  
Outlet Obstruction ◽  
Bladder Capacity ◽  
Sprague Dawley ◽  
Stress Markers ◽  
Bladder Cell ◽  
Sprague Dawley Rats ◽  
Antioxidant Proteins

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.

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 ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Rat Model ◽  
Bladder Outlet Obstruction ◽  
Bladder Dysfunction ◽  
Outlet Obstruction ◽  
Epigallocatechin Gallate ◽  
Saline Control ◽  
Tunel Staining ◽  
Sprague Dawley

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.

Effects of Lead Nitrate Induced Histological Changes in Liver of Male Sprague Dawley Rats

2021 ◽  
Vol 15 (11) ◽  
pp. 2948-2950
Author(s):  
Sumaira Abbasi ◽  
Mushtaq Ahmad ◽  
Kaukab Anjum ◽  
Amaidah Mir ◽  
Ayesha Irfan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Lead Nitrate ◽  
Normal Diet ◽  
The Body ◽  
Central Vein ◽  
Sprague Dawley ◽  
Toxic Agent ◽  
Sprague Dawley Rats ◽  
Group B

Lead is a highly toxic agent and a potent risk factor for various diseases as its quantity in an environment is increasing day by day. Aim: To observe and analyze the lead nitrate induced histomorphological changes in the liver of Sprague Dawley rats. Study Design: Experimental Study. Methodology: Animals of group A (control) were fed on normal diet but the animals of group B were given 50mg/kg of lead nitrate dissolved in 10ml of distilled water through oral gavage for 14 days daily. SPSS version 22 was used for data analysis. All the quantitative data was expressed as means ± SD. One Way ANOVA followed by Post Hoc Tukey test was applied. Results: Degenerative effects were noted. The number of Inflammatory and Kupfffer cells is increased with decreased in the body weight. Steatosis and central vein congestion were also present. Conclusion: It was concluded that degenerative effects histologically may be due to oxidative stress produced by formation of free radicals and denaturation of proteins by lead nitrate. Keywords: Lead, Liver, Central Vein Congestion, Oxidative Stress and Free Radicals.

Biochemical changes and oxidative stress induced by zearalenone in the liver of pregnant rats

2014 ◽  
Vol 34 (1) ◽  
pp. 65-73 ◽  
Author(s):  
C Zhou ◽  
Y Zhang ◽  
S Yin ◽  
Z Jia ◽  
A Shan
Keyword(s):  
Oxidative Stress ◽  
Messenger Rna ◽  
Experimental Period ◽  
Normal Diet ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Sprague Dawley Rats ◽  
Albumin Content ◽  
Dose Dependent

The aim of the present research was to examine the toxic influence of different doses of zearalenone (ZEN) on the liver, especially oxidative stress induced by ZEN on the liver. A total of 48 pregnant Sprague-Dawley rats were randomly assigned into 4 treatments groups with 12 animals in each. The rats were fed with a normal diet treated with 0 mg/kg (control), 50 mg/kg (treatment 1), 100 mg/kg (treatment 2), or 150 mg/kg (treatment 3) ZEN in feed on gestation days (GDs) 0–7 and then all the rats were fed with a normal diet on GDs 8–20. The experimental period lasted 21 days. The results showed that exposure to ZEN induced increase in aspartate amino transferase, alanine aminotransferase, and alkaline phosphatase activities and decrease in total protein and albumin content in a dose-dependent manner and also induce decrease in superoxide dismutase and glutathione peroxidase activities and increase in malondialdehyde content in a dose-dependent manner in the serum and the liver. The increased transcription of cytochrome P450 2E1 (CYP2E1) was detected in the liver after exposure to ZEN. These results suggested that ZEN not only caused damage in the liver of pregnant rats in a dose-dependent manner but also induced the messenger RNA expression of CYP2E1 in the liver.

Protective effect of astaxanthin on acute cerebral infarction in rats

2017 ◽  
Vol 37 (9) ◽  
pp. 929-936 ◽  
Author(s):  
Yu Nai ◽  
Hong Liu ◽  
Xizhuang Bi ◽  
Hongyu Gao ◽  
Chao Ren
Keyword(s):  
Oxidative Stress ◽  
Cerebral Infarction ◽  
Cerebral Edema ◽  
Acute Cerebral Infarction ◽  
Group Model ◽  
Model Group ◽  
Sprague Dawley ◽  
Rt Pcr ◽  
Stress Markers ◽  
Sprague Dawley Rats

The aim of the study was to investigate the effect of astaxanthin and its possible mechanisms on acute cerebral infarction (ACI) in rat model. Male Sprague Dawley rats were randomly divided into sham group, model group, and astaxanthin-treated groups (20, 40, and 80 mg/kg). Neurological examination, the ratio of cerebral edema, and histopathology changes were assessed. Moreover, some oxidative stress markers were obtained for biochemical analysis, and the expression of neurotrophic factors gene was detected by real-time polymerase chain reaction (RT-PCR) method. The results showed that treatment with astaxanthin notably reduced neurological deficit scores and the ratio of cerebral edema compared with the model group. Meanwhile, astaxanthin increased the activity of catalase, superoxide dismutase, and glutathioneperoxidase as well as decreased the content of malondialdehyde in brain tissue. RT-PCR results showed that the expression of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) mRNA were increased with astaxanthin treatment. The results indicated that astaxanthin could ameliorate ACI followed by suppressing oxidative stress and upregulating the expression of BDNF and NGF mRNA.

scholarly journals Glutathione Supplementation Attenuates Oxidative Stress and Improves Vascular Hyporesponsiveness in Experimental Obstructive Jaundice

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Jiaying Chen ◽  
Feixiang Wu ◽  
Yue Long ◽  
Weifeng Yu
Keyword(s):  
Oxidative Stress ◽  
Obstructive Jaundice ◽  
Isometric Tension ◽  
Serum Total Bilirubin ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Stress Markers ◽  
Sprague Dawley Rats ◽  
Duct Ligation ◽  
Group A

We investigated the protective effects and mechanism of glutathione (GSH) on vascular hyporesponsiveness induced by bile duct ligation (BDL) in a rat model. Seventy-two male Sprague-Dawley rats were randomly divided into four groups: a NS group, a GSH group, a BDL + NS group, and a BDL + GSH group. GSH was administrated into rats in the GSH and BDL + GSH groups by gastric gavage. An equal volume of normal saline was, respectively, given in the NS group and BDL + NS group. Blood was gathered for serological determination and thoracic aorta rings were isolated for measurement of isometric tension. Obstructive jaundice led to a significant increase in the serum total bilirubin, AST, and ALT levels. The proinflammatory cytokines levels (TNF-αand IL-1β), concentration of NO, and oxidative stress markers (MDA and 3-NT) were increased as well. All of those were reduced by the treatment of GSH. Meanwhile, contraction of aorta rings to NA and vasorelaxation to ACh or SNP in the BDL group rats were markedly decreased, while GSH administration reversed this change. Our findings suggested that GSH supplementation attenuated overexpressed ONOO(−) from the reaction of excessive NO withO2∙-and protected against obstructive jaundice-induced vascular hyporesponsiveness in rats.

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