scholarly journals Sacran, a High-molecular Weight Polysaccharide Inhibits Renal Injury and Oxidative Stress in Chronic Renal Failure Model Rats

2018 ◽  
Vol 4 (2) ◽  
pp. 267-275
Author(s):  
Miwa Goto ◽  
Daisuke Iohara ◽  
Shinichiro Kaneko ◽  
Taishi Higashi ◽  
Keiichi Motoyama ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Treatment Group ◽  
Renal Injury ◽  
Subsequent Development ◽  
Systemic Circulation ◽  
Failure Model ◽  
Similar Treatment ◽  
Nitrogen Levels ◽  
And Oxidative Stress ◽  
Carbonaceous Adsorbent

The administration of a high-molecular polysaccharide Sacran results in a significant decrease in renal injury and oxidative stress, compared with that for the oral carbonaceous adsorbent, AST-120 (Kremezin®) or a non-treatment group in 5/6 nephrectomized rats. An oral administration of Sacran (20 mg/day) over a 4 week period resulted in a significant decrease in serum indoxyl sulfate, creatinine and urea nitrogen levels, compared with a similar treatment with AST-120 or the non-treatment group. Sacran treatment also resulted in antioxidant potential being maintained, compared with that for AST-120 or the non-treatment group. Immuno-histochemical analyses also demonstrated that CRF rats, when treated with Sacran, showed a decrease in the level of accumulated renal fibrosis and 8-OHdG compared with AST-120 or the non-treatment group. These results suggest that the ingestion of Sacran results in a significant reduction in the levels of prooxidants, such as uremic toxins, in the gastrointestinal tract, thereby inhibiting the subsequent development of oxidative stress in the systemic circulation.

An oral absorbent, surface-deacetylated chitin nano-fiber ameliorates renal injury and oxidative stress in 5/6 nephrectomized rats

2017 ◽  
Vol 161 ◽  
pp. 21-25 ◽  
Author(s):  
Makoto Anraku ◽  
Ryo Tabuchi ◽  
Shinsuke Ifuku ◽  
Tomone Nagae ◽  
Daisuke Iohara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Nano Fiber ◽  
And Oxidative Stress

Abstract 371: DPPIV Inhibitor MK0626 Prevents Western Diet Induced Renal Injury via Suppression of Kidney Tissue Ras

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Ravi Nistala ◽  
Javad Habibi ◽  
Annayya Aroor ◽  
Melvin R Hayden ◽  
Mona Garro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Renal Injury ◽  
Sodium Excretion ◽  
The United States ◽  
Western Diet ◽  
Ang Ii ◽  
High Fructose ◽  
Dppiv Inhibitor ◽  
And Oxidative Stress

Objectives: Obesity is an independent risk factor for development and progression of renal injury. High fructose corn syrup consumption has coincided with the obesity epidemic in the United States. High fructose (60%) diets have been demonstrated to be associated with elevation in BP and worsening insulin resistance along with renal injury via increased hepatic production of uric acid. Recently, DPPIV inhibitors have been shown to improve diabetic changes and sodium excretion, effects that are beyond glycemic control. Therefore, the renal protective benefits of DPPIV inhibition in a clinically relevant Western diet fed mouse model were examined. Methods: Mice fed a high fat/high fructose (WD) diet for 16 weeks and given a DPPIV inhibitor MK0626 in their diet were examined for metabolic parameters, inflammation, kidney renin-angiotensin system (RAS) and oxidative stress. Renal injury was assessed by biochemical, immunohistological and electron microscopy techniques. In vitro , angiotensin II (Ang II) effects on OKP-PTCs were assessed for mechanism. Results: MK0626 ameliorated WD-induced increases in serum uric acid, oxidative stress and RAS. WD induced suppression of IL-10 was reversed by MK0626. There was a tendency to improve HOMA-IR by MK0626 but no effect on BP and body weights. Diet induced DPPIV activation in the plasma and kidney of WD mice was abrogated by MK0626 (~80%). WD mice were characterized by increased proteinuria (~3-fold), mesangial expansion and podocyte effacement and these changes were prevented by MK0626. In addition, the PTC endocytosis protein megalin and basilar canalicular network and mitochondrial ultrastructure abnormalities were reversed by MK0626. WD mice had decreased sodium excretion which was improved by MK0626. Ang II directly increased DPPIV activity and sodium hydrogen exchanger activity in PTCs and decreased megalin protein, which was effectively prevented by MK0626. Conclusion: Thus, WD induced increases in DPPIV activity is associated with elevations in uric acid, renal RAS, inflammation and oxidative stress which may result in renal injury. These results suggest that DPPIV inhibitors prevent WD induced renal injury and offer a novel therapy for diabetic and obesity associated renal disease.

scholarly journals Hydrogen Gas Alleviates Chronic Intermittent Hypoxia-Induced Renal Injury through Reducing Iron Overload

Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1184 ◽  
Author(s):  
Peng Guan ◽  
Zhi-Min Sun ◽  
Li-Fei Luo ◽  
Ya-Shuo Zhao ◽  
Sheng-Chang Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Iron Overload ◽  
Renal Injury ◽  
Intermittent Hypoxia ◽  
Hydrogen Gas ◽  
Chronic Intermittent Hypoxia ◽  
Protective Effects ◽  
Divalent Metal Transporter 1 ◽  
Divalent Metal Transporter ◽  
And Oxidative Stress

Iron-induced oxidative stress has been found to be a central player in the pathogenesis of kidney injury. Recent studies have indicated H2 can be used as a novel antioxidant to protect cells. The present study was designed to investigate the protective effects of H2 against chronic intermittent hypoxia (CIH)-induced renal injury and its correlation mechanism involved in iron metabolism. We found that CIH-induced renal iron overloaded along with increased apoptosis and oxidative stress. Iron accumulates mainly occurred in the proximal tubule epithelial cells of rats as showed by Perl’s stain. Moreover, we found that CIH could promote renal transferrin receptor and divalent metal transporter-1 expression, inhibit ceruloplasmin expression. Renal injury, apoptosis and oxidative stress induced by CIH were strikingly attenuated in H2 treated rats. In conclusion, hydrogen may attenuate CIH-induced renal injury at least partially via inhibiting renal iron overload.

Salt sensitivity in experimental thyroid disorders in rats

2011 ◽  
Vol 301 (2) ◽  
pp. E281-E287 ◽  
Author(s):  
Rocío Perez-Abud ◽  
Isabel Rodríguez-Gómez ◽  
Ana Belén Villarejo ◽  
Juan Manuel Moreno ◽  
Rosemary Wangensteen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Salt Intake ◽  
Salt Sensitivity ◽  
High Salt ◽  
Thyroid Disorders ◽  
High Salt Intake ◽  
Male Wistar Rats ◽  
Experimental Thyroid ◽  
And Oxidative Stress

This study assessed salt sensitivity, analyzing the effects of an increased saline intake on hemodynamic, morphological, and oxidative stress and renal variables in experimental thyroid disorders. Six groups of male Wistar rats were used: control, hypothyroid, hyperthyroid, and the same groups treated with salt (8% via food intake). Body weight, blood pressure (BP), and heart rate (HR) were recorded weekly for 6 wk. Finally, BP and HR were recorded directly, and morphological, metabolic, plasma, and renal variables were measured. High-salt intake increased BP in thyroxine-treated rats but not in control or hypothyroid rats. High-salt intake increased cardiac mass in all groups, with a greater increase in hyperthyroid rats. Urinary isoprostanes and H2O2 were higher in hyperthyroid rats and were augmented by high-salt intake in all groups, especially in hyperthyroid rats. High-salt intake reduced plasma thyroid hormone levels in hyperthyroid rats. Proteinuria was increased in hyperthyroid rats and aggravated by high-salt intake. Urinary levels of aminopeptidases (glutamyl-, alanyl-, aspartyl-, and cystinylaminopeptidase) were increased in hyperthyroid rats. All aminopeptidases were increased by salt intake in hyperthyroid rats but not in hypothyroid rats. In summary, hyperthyroid rats have enhanced salt sensitivity, and high-salt intake produces increased BP, cardiac hypertrophy, oxidative stress, and signs of renal injury. In contrast, hypothyroid rats are resistant to salt-induced BP elevation and renal injury signs. Urinary aminopeptidases are suitable biomarkers of renal injury.

Beneficial effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin in rats

2015 ◽  
Vol 35 (3) ◽  
pp. 276-281 ◽  
Author(s):  
H Elbe ◽  
Z Dogan ◽  
E Taslidere ◽  
A Cetin ◽  
Y Turkoz
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Tissue ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Histopathological Changes ◽  
Tubular Atrophy ◽  
Beneficial Effects ◽  
Wistar Albino Rats ◽  
And Oxidative Stress

Ciprofloxacin is a broad-spectrum quinolone antibiotic commonly used in clinical practice. Quercetin is an antioxidant belongs to flavonoid group. It inhibits the production of superoxide anion. In this study, we aimed to evaluate the effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin. Twenty-eight female Wistar albino rats were divided into four groups: control, quercetin (20 mg kg−1 day−1 gavage for 21 days), ciprofloxacin (20 mg kg−1 twice a day intraperitoneally for 10 days), and ciprofloxacin + quercetin. Samples were processed for histological and biochemical evaluations. Malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), and catalase (CAT) activities were measured in kidney tissue. The ciprofloxacin group showed histopathological changes such as infiltration, dilatation in tubules, tubular atrophy, reduction of Bowman’s space, congestion, hemorrhage, and necrosis. In the ciprofloxacin + quercetin group, these histopathological changes markedly reduced. MDA levels increased in the ciprofloxacin group and decreased in the ciptofloxacin + quercetin group. SOD and CAT activities and GSH levels significantly decreased in the ciprofloxacin group. On the other hand, in the ciprofloxacin + quercetin group, SOD and CAT activities and GSH levels significantly increased with regard to the ciprofloxacin group. We concluded that quercetin has antioxidative and therapeutic effects on renal injury and oxidative stress caused by ciprofloxacin in rats.

scholarly journals Mitochondrial dysfunction and oxidative stress are involved in the mechanism of tramadol-induced renal injury

2021 ◽  
pp. 100049
Author(s):  
Khadijah Mousavi ◽  
Ram Kumar Manthari ◽  
Asma Najibi ◽  
Zhipeng Jia ◽  
Mohammad Mehdi Ommati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Renal Injury ◽  
And Oxidative Stress

scholarly journals Amelioration of Renal Injury and Oxidative Stress by the nNOS Inhibitor L-VNIO in the Salt-sensitive mRen2.Lewis Congenic Rat

2012 ◽  
Vol 59 (6) ◽  
pp. 529-538 ◽  
Author(s):  
Liliya M. Yamaleyeva ◽  
Sarah H. Lindsey ◽  
Jasmina Varagic ◽  
Li Li Zhang ◽  
Patricia E. Gallagher ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
And Oxidative Stress

scholarly journals Prior intake of Brazil nuts attenuates renal injury induced by ischemia and reperfusion

2018 ◽  
Vol 40 (1) ◽  
pp. 10-17 ◽  
Author(s):  
Natassia Alberici Anselmo ◽  
Leticia Colombo Paskakulis ◽  
Renata Correia Garcias ◽  
Fernanda Fortuci Resende Botelho ◽  
Giovana Queda Toledo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Function ◽  
Creatinine Clearance ◽  
Renal Injury ◽  
Ischemia Reperfusion ◽  
Antioxidant Properties ◽  
Kidney Injury ◽  
Urinary Output ◽  
Left Renal Artery ◽  
And Oxidative Stress

ABSTRACT Introduction: Ischemia-reperfusion (IR) injury results from inflammation and oxidative stress, among other factors. Because of its anti-inflammatory and antioxidant properties, the Brazil nut (BN) might attenuate IR renal injury. Objective: The aim of the present study was to investigate whether the intake of BN prevents or reduces IR kidney injury and inflammation, improving renal function and decreasing oxidative stress. Methods: Male Wistar rats were distributed into six groups (N=6/group): SHAM (control), SHAM treated with 75 or 150 mg of BN, IR, and IR treated with 75 or 150 mg of BN. The IR procedure consisted of right nephrectomy and occlusion of the left renal artery with a non-traumatic vascular clamp for 30 min. BN was given daily and individually for 7 days before surgery (SHAM or IR) and maintained until animal sacrifice (48h after surgery). We evaluated the following parameters: plasma creatinine, urea, and phosphorus; proteinuria, urinary output, and creatinine clearance; plasmatic TBARS and TEAC; kidney expression of iNOS and nitrotyrosine, and macrophage influx. Results: Pre-treatment with 75 mg of BN attenuated IR-induced renal changes, with elevation of creatinine clearance and urinary output, reducing proteinuria, urea, and plasmatic phosphorus as well as reducing kidney expression of iNOS, nitrotyrosine, and macrophage influx. Conclusion: Low intake of BN prior to IR-induced kidney injury improves renal function by inhibition of macrophage infiltration and oxidative stress.

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