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LPS-induced renal inflammation is prevented by (−)‐epicatechin in rats

This work investigated the capacity of (−)-epicatechin to prevent the renal damage induced by LPS administration in rats. Male Sprague Dawley rats were fed for 4 days a diet without or with supplementation with (−)-epicatechin (80mg/kg BW/d), and subsequently i.p. injected with lipopolysaccharide (L...

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Published in:Redox biology 2017-04, Vol.11, p.342-349
Main Authors: Prince, Paula Denise, Fischerman, Laura, Toblli, Jorge E., Fraga, Cesar G., Galleano, Monica
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description This work investigated the capacity of (−)-epicatechin to prevent the renal damage induced by LPS administration in rats. Male Sprague Dawley rats were fed for 4 days a diet without or with supplementation with (−)-epicatechin (80mg/kg BW/d), and subsequently i.p. injected with lipopolysaccharide (LPS). Six hours after injection, LPS-treated rats exhibited increased plasma creatinine and urea levels as indicators of impaired renal function. The renal cortex of the LPS-treated rats showed: i) increased expression of inflammatory molecules (TNF-α, iNOS and IL-6); ii) activation of several steps of NF-κB pathway; iii) overexpression of TLR4, and iv) higher superoxide anion production and lipid peroxidation index in association with increased levels of gp91phox and p47phox (NOX2) and NOX4. Pretreatment with dietary (−)-epicatechin prevented the adverse effects of LPS challenge essentially by inhibiting TLR4 upregulation and NOX activation and the consequent downstream events, e.g. NF-kB activation.
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Male Sprague Dawley rats were fed for 4 days a diet without or with supplementation with (−)-epicatechin (80mg/kg BW/d), and subsequently i.p. injected with lipopolysaccharide (LPS). Six hours after injection, LPS-treated rats exhibited increased plasma creatinine and urea levels as indicators of impaired renal function. The renal cortex of the LPS-treated rats showed: i) increased expression of inflammatory molecules (TNF-α, iNOS and IL-6); ii) activation of several steps of NF-κB pathway; iii) overexpression of TLR4, and iv) higher superoxide anion production and lipid peroxidation index in association with increased levels of gp91phox and p47phox (NOX2) and NOX4. 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subjects Administration, Oral
Animals
Anti-Inflammatory Agents - pharmacology
Antioxidants - pharmacology
Catechin - pharmacology
Creatinine - blood
Endotoxemia
Flavonoids
Gene Expression Regulation
Injections, Intraperitoneal
Interleukin-6 - genetics
Interleukin-6 - immunology
Kidney - drug effects
Kidney - immunology
Kidney - pathology
Lipopolysaccharides
Male
NADPH Oxidase 2 - genetics
NADPH Oxidase 2 - immunology
NADPH Oxidase 4 - genetics
NADPH Oxidase 4 - immunology
NADPH Oxidases - genetics
NADPH Oxidases - immunology
Nephritis - chemically induced
Nephritis - genetics
Nephritis - pathology
Nephritis - prevention & control
NF-kappa B - genetics
NF-kappa B - immunology
Nitric Oxide Synthase Type II - genetics
Nitric Oxide Synthase Type II - immunology
Rats
Rats, Sprague-Dawley
Reactive oxygen species
Renopathies
Research Paper
Signal Transduction
Toll-Like Receptor 4 - genetics
Toll-Like Receptor 4 - immunology
Toll-like receptors
Tumor Necrosis Factor-alpha - genetics
Tumor Necrosis Factor-alpha - immunology
Urea - blood
title LPS-induced renal inflammation is prevented by (−)‐epicatechin in rats
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