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Resveratrol, curcumin and gallic acid attenuate glyoxal-induced damage to rat renal cells

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Autore
Hashemzaei M., Tabrizian K., Alizadeh Z., Pasandideh S., Rezaee R., Mamoulakis C., Tsatsakis A., Skaperda Z., Kouretas D., Shahraki J.
Data
2020
Language
en
DOI
10.1016/j.toxrep.2020.11.008
Soggetto
chloroquine
curcumin
dimethyl sulfoxide
gallic acid
glutamine
glyoxal
mannitol
reactive oxygen metabolite
resveratrol
thiobarbituric acid reactive substance
animal cell
animal experiment
animal model
antioxidant activity
apoptosis
Article
cell viability
controlled study
cytotoxicity
diabetes mellitus
diabetic nephropathy
EC50
kidney injury
lipid peroxidation
lipid peroxidation assay
lysosome membrane
male
mitochondrial membrane potential
mitochondrial permeability
nonhuman
oxidative stress
rat
spectrofluorometry
trypan blue assay
Elsevier Inc.
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Abstract
Glyoxal (GO), a by-product of glucose auto-oxidation, is involved in the glycation of proteins/ lipids and formation of advanced glycation (AGE) and lipoxidation (ALE) end products. AGE/ALE were shown to contribute to diabetic complications development/progression such as nephropathy. Diabetic nephropathy progression has an oxidative nature. Given the antioxidant effects of polyphenols, potential protective effects of resveratrol, curcumin and gallic acid, in rat renal cells treated with GO, were evaluated in the present work. According to our results, incubation of GO with the cells reduced their viability and led to membrane lysis, reactive oxygen species (ROS) formation, lipid peroxidation, mitochondrial membrane potential collapse, and lysosomal membrane leakage. These findings were prevented by pre-treatment with resveratrol, curcumin and gallic acid. Mitochondrial and lysosomal toxic interactions appear to worsen oxidative stress/cytotoxicity produced by GO. Resveratrol, curcumin and gallic acid inhibited ROS formation and attenuated GO-induced renal cell death. © 2020 The Author(s)
URI
http://hdl.handle.net/11615/73925
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  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19735]
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