Nebivolol prevents ethanol-induced reactive oxygen species generation and lipoperoxidation in the rat kidney by regulating NADPH oxidase activation and expression

Vale, Gabriel Tavares do; Gonzaga, Natália A.; Simplicio, Janaina A.; Tirapelli, Carlos Renato

doi:10.1016/j.ejphar.2017.01.036

Cited by 24 publications

(12 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, the antioxidant effect of nebivolol on the kidney may vary depending on the model. For example, nebivolol reduced both renal NOX2 and NOX4 expressions in the Zucker obese (ZO) fa/fa rat, but only prevented NOX2 in ethanol‐induced kidney OS …”

Section: Discussionmentioning

confidence: 99%

Nebivolol ameliorated kidney damage in Zucker diabetic fatty rats by regulation of oxidative stress/NO pathway: Comparison with captopril

Wang

Zhang

et al. 2018

Clin Exp Pharma Physio

View full text Add to dashboard Cite

The aim was to evaluate the effects and mechanisms of nebivolol on renal damage in Zucker diabetic fatty (ZDF) rats, in comparison with those of atenolol and captopril. Animals were divided into: control lean Zucker rats, ZDF rats, ZDF rats orally treated with nebivolol (10 mg/kg), atenolol (100 mg/kg) or captopril (40 mg/kg) for 6 months. Systolic blood pressure (SBP), blood glucose, kidney structure and function, plasma and kidney levels of nitric oxide (NO) and asymmetric dimethylarginine (ADMA), and oxidant status were evaluated. Kidney expressions of adenosine monophosphate-activated protein kinase (AMPK), NADPH oxidase (NOX) isoforms 2 and 4 and subunit p22 , nitric oxide synthase (NOS) isoforms, endothelial NOS (eNOS) uncoupling, protein arginine N-methyltransferase (PRMT) 1, and dimethylarginine dimethylaminohydrolase (DDAH) 1 and 2 were tested. All drugs induced a similar control of SBP. Nebivolol did not affect the increased plasma glucose. Unlike atenolol, nebivolol prevented the decrease in plasma insulin, and, like captopril, it reduced plasma lipid contents. Nebivolol ameliorated, to a greater extent than captopril, damages to renal structure and function, which were associated with an improvement in interlobular artery dysfunction. Nebivolol elevated kidney phosphorylation of AMPK, attenuated NOX4 and p22 expression and oxidative stress marker levels. Nebivolol increased plasma and renal NO, enhanced expressions of eNOS, p-eNOS and neuronal NOS, and suppressed eNOS uncoupling and inducible NOS expression. High ADMA in plasma and kidney were decreased by nebivolol through increasing DDAH2 and decreasing protein arginine N-methyltransferase 1. Long-term treatment of nebivolol ameliorated diabetic nephropathy, at least in part, via regulation of renal oxidative stress/NO pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Nebivolol ameliorated kidney damage in Zucker diabetic fatty rats by regulation of oxidative stress/NO pathway: Comparison with captopril

Wang

Zhang

et al. 2018

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

“…In the kidneys, ROS is generated via both enzymatic and non-enzymatic processes [22,23,27,32,36,37]. In pathophysiological conditions, ROS, such as O 2− , may react with nitric oxide (NO) to produce ONOO − , which is a highly oxidizing compound that reacts with biological molecules, causing lipoperoxidation [25,38,39] and oxidation of proteins [40], cytomembrane, and DNA [32,37] in the kidneys. In addition, Das et al reported that alcohol consumption impairs the ability of CAT to catalyze the decomposition of H 2 O 2 in the kidneys [41].…”

Section: Effects Of Ethanol On the Kidneysmentioning

confidence: 99%

Alcohol Consumption Can be a “Double-Edged Sword” for Chronic Kidney Disease Patients

Fan

Yun

et al. 2019

Med Sci Monit

View full text Add to dashboard Cite

Excessive drinking of alcohol is becoming a worldwide problem, and people have recognized that there exists a close relationship between chronic kidney disease (CKD) and alcohol consumption. However, there are many inconsistencies between experimental and clinical studies on alcohol consumption and kidney damage. The possible reason for this contradictory conclusion is the complex drinking pattern of humans and some bioactivators in wine. In addition, the design itself of the clinical studies can also produce conflicting interpretations of the results. Considering the benefits of light-to-moderate alcohol consumption, we recommend that CKD patients continue light-to-moderate drinking, which is beneficial to them. Because alcohol consumption can lead to adverse events, we do not advise non-drinkers to start to drink. Although light-to-moderate alcohol consumption may not pose a risk to patients with CKD, the patients’ condition needs to be considered. Consumption of even small amounts of alcohol can be associated with increased death risk. Additional clinical and experimental studies are needed to clarify the effect of alcohol on the kidneys and alcohol consumption on CKD patients.

show abstract

“…[26] indicated that advanced oxidation protein products decrease expression of nephrin and podocin in podocytes through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent reactive oxygen species generation that activated p38 mitogen-activated protein kinase pathway. Interestingly, previous studies had demonstrated that ethanol exposure led to increase the level of NADPH oxidase in the kidney tissue, as well as in the cardiac tissue concurrent alteration of fetal gene expression [15, 27, 28]. Based on the results of this study and the previous ones, we suggest that ethanol induces NADPH oxidase to mediate oxidative stress, may trigger decreasing expression of nephrin and podocin in podocytes, and contribute, at least in part, to glomerular disease and kidney injury.…”

Section: Discussionmentioning

confidence: 99%

Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats

Samadi

Shirpoor

Afshari

et al. 2018

IMAS

View full text Add to dashboard Cite

BackgroundChronic alcohol ingestion-induced kidney structure and function alterations are very well known, but the precise underlying molecular mediators involved in ethanol-induced kidney abnormalities remain elusive. The aim of this study was to investigate the effect of chronic ethanol exposure on matrix metalloproteinase 2, 9 (MMP), glomerular filtration barrier proteins (nephrin and podocin), as well as vascular endothelial growth factor receptor 1, 2 (VEGFRs) isoforms gene expression in the kidney of rats.MethodsSixteen male Wistar rats with an initial body weight of 220 ± 10 g were divided into the following two groups: (1) control and (2) ethanol (4.5 g/kg BW).ResultsAfter 6 weeks of treatment, the results revealed a significant increase in isoforms VEGFR1 and VEGFR2 of VEGFR gene expression, significant increases of MMP2 and MMP9 activities, as well as significant decrease of nephrin and podocin gene expressions in the ethanol group, compared with that in the control group.ConclusionThese findings indicate that ethanol-induced kidney abnormalities may be in part associated with alteration in expressions of VEGFRs, nephrin, and podocin and in increasing activities of MMP2 and MMP9 as key molecular mediators in the kidney function.

show abstract

Nebivolol prevents ethanol-induced reactive oxygen species generation and lipoperoxidation in the rat kidney by regulating NADPH oxidase activation and expression

Cited by 24 publications

References 35 publications

Nebivolol ameliorated kidney damage in Zucker diabetic fatty rats by regulation of oxidative stress/NO pathway: Comparison with captopril

Nebivolol ameliorated kidney damage in Zucker diabetic fatty rats by regulation of oxidative stress/NO pathway: Comparison with captopril

Alcohol Consumption Can be a “Double-Edged Sword” for Chronic Kidney Disease Patients

Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats

Contact Info

Product

Resources

About