Quercetin ameliorates Di (2-ethylhexyl) phthalate-induced nephrotoxicity by inhibiting NF-κB signaling pathway.
Di (2-ethylhexyl) phthalate
HEK293 cell line
mitochondria
nephrotoxicity
nuclear factor kappa B
quercetin
Journal
Toxicology research
ISSN: 2045-452X
Titre abrégé: Toxicol Res (Camb)
Pays: England
ID NLM: 101587950
Informations de publication
Date de publication:
Apr 2022
Apr 2022
Historique:
received:
04
07
2021
revised:
10
01
2022
accepted:
21
01
2022
entrez:
5
5
2022
pubmed:
6
5
2022
medline:
6
5
2022
Statut:
epublish
Résumé
This study aimed to evaluate the possible protective effects of quercetin, a natural flavonoid, against nephrotoxicity induced by Di (2-ethylhexyl) phthalate (DEHP) in kidney tissue of rats and human embryonic kidney (HEK) 293 cell line. The HEK-293 cells were treated with different concentrations of quercetin 24 h before treatment with monoethylhexyl phthalate (MEHP). Male rats were treated with 200-mg/kg DEHP, 200-mg/kg DEHP plus quercetin (50 and 100 mg/kg), and 200-mg/kg DEHP plus vitamin E (20 mg/kg) for 45 days by gavage. Quercetin treatment reduced cytotoxicity and oxidative damage inducing by MEHP in HEK-293 cells. The in vivo findings showed that 100-mg/kg quercetin significantly suppressed DEHP-induced kidney damage. For exploring the involved mechanisms, the expressions of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), nuclear factor kappa B (NFκB), and tumor necrosis factor alpha (TNFα) genes were determined via real-time Polymerase chain reaction (PCR) assay. High dose of quercetin significantly decreased the gene expressions of NF-κB and TNFα, whereas the alternations of Nrf2 and HO-1 gene expressions were not significant in quercetin groups in compared with DEHP group. These findings suggested that the suppression of DEHP-induced nephrotoxicity via quercetin is correlated, at least in part, with its potential to regulate NF-κB signaling pathway.
Identifiants
pubmed: 35510228
doi: 10.1093/toxres/tfac006
pii: tfac006
pmc: PMC9052324
doi:
Types de publication
Journal Article
Langues
eng
Pagination
272-285Informations de copyright
© The Author(s) 2022. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
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