Uraemic toxin‐induced inflammation and oxidative stress in human endothelial cells: protective effect of polyphenol‐rich extract from açaí
Autor: | Patricia Leticia Trindade, Angela Castro Resende, Graziele Freitas de Bem, Christophe O. Soulage, Julio Beltrame Daleprane, Elaine Soares, Magna Cottini Fonseca Passos, Elisa B. Monteiro |
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Přispěvatelé: | Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN), Institut National de la Recherche Agronomique (INRA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hospices Civils de Lyon (HCL), Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Institut National de la Recherche Agronomique (INRA) |
Rok vydání: | 2020 |
Předmět: |
Acai
Necrosis Euterpe Physiology [SDV]Life Sciences [q-bio] uremic toxins Inflammation 030204 cardiovascular system & hematology Pharmacology Protective Agents medicine.disease_cause Antioxidants endothelial dysfunction Superoxide dismutase 03 medical and health sciences 0302 clinical medicine Physiology (medical) Human Umbilical Vein Endothelial Cells medicine Humans oxidative stress Secretion Viability assay Renal Insufficiency Chronic Endothelial dysfunction Cells Cultured Nutrition and Dietetics Cell Death biology Plant Extracts Superoxide Dismutase Chemistry Polyphenols General Medicine medicine.disease Endothelial stem cell inflammation biology.protein Cytokines medicine.symptom Biomarkers chronic kidney disease 030217 neurology & neurosurgery Oxidative stress |
Zdroj: | Exp. Physiol. Exp. Physiol., 2019, ⟨10.1113/ep088080⟩ |
ISSN: | 1469-445X 0958-0670 |
DOI: | 10.1113/ep088080 |
Popis: | NEW FINDING: What is the central question of this study? Polyphenols shows protective cardiometabolic actions in different disease models. A potential role of a polyphenols-rich extract from acai in preventing uremic toxin-induced endothelial dysfunction in endothelial cells has not been previously reported. What is the main finding and its importance? We showed that polyphenols from acai prevented cell death, restored the migratory capacity, protected from inflammation and contributed to antioxidant response restoration in endothelial cells exposed to uremic toxins. The protective role of acai from toxic effects exerted by uremic toxins presents a potential new therapeutic target in endothelial cells. ABSTRACT: Aims In chronic kidney disease (CKD), progressive loss of kidney function results in the accumulation of protein-bound uremic toxins such as p-cresyl-sulfate (p-CS) and indoxyl sulfate (IS). Among strategies to ameliorate uremic toxin harmful actions, phenolic compounds have been extensively studied. The main goal of this work was to evaluate the antioxidant and anti-inflammatory actions of phenolic-rich acai seed extract (ASE), in response to endothelial dysfunction induced by IS and p-CS, in human umbilical vein endothelial cells (HUVEC). Main methods Cells were treated with ASE (10 mug/mL) in the presence or absence of IS (61 mug/mL) and p-CS (40 mug/mL). Cell viability, cell death, cell migratory capacity and inflammatory biomarker expression were evaluated. Cellular antioxidant response was measured through the activity and expression of antioxidant enzymes and oxidative damage was evaluated. Key findings IS and p-CS lowered cell viability, triggered cell death and lowered the migratory capacity in endothelial cells (p \textless 0.05). ASE prevented cell death and restored the migratory capacity in cells exposed to IS. Both toxins up-regulated pro-inflammatory cytokine expression and ASE was able to beneficially counteract this effect. TNF-alpha secretion was greater in uremic toxins treated cells and ASE reversed this phenomenon in cells treated with both toxins concomitantly (p \textless 0.05). Regarding the antioxidant response, superoxide dismutase expression was strikingly lower in cells treated with both toxins, and ASE inhibited this harmful effect (p \textless 0.05). Significance From the results above, we conclude that ASE exerted protective effects on inflammation and oxidative stress caused by uremic toxins (particularly by IS) in human endothelial cells. This article is protected by copyright. All rights reserved. |
Databáze: | OpenAIRE |
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