Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response

Diclofenac (DIC) is an NSAID that can cause toxic effects in animals and humans and carvacrol (CAR) is a monoterpene compound that displays effective pharmacological and biological actions. The purpose of this work was to assess the influences of CAR on DIC-induced renal injury and oxidative stress...

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Autores principales: Ali Nouri, Farzad Izak-Shirian, Vahideh Fanaei, Maryam Dastan, Mahdieh Abolfathi, Alireza Moradi, Mansoor Khaledi, Hamzeh Mirshekari-Jahangiri
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Publicado: Elsevier 2021
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spelling oai:doaj.org-article:b80a16b774f84adab6ab7caa39e9cd512021-12-02T05:02:49ZCarvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response2405-844010.1016/j.heliyon.2021.e08358https://doaj.org/article/b80a16b774f84adab6ab7caa39e9cd512021-11-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2405844021024610https://doaj.org/toc/2405-8440Diclofenac (DIC) is an NSAID that can cause toxic effects in animals and humans and carvacrol (CAR) is a monoterpene compound that displays effective pharmacological and biological actions. The purpose of this work was to assess the influences of CAR on DIC-induced renal injury and oxidative stress in male rats. The rats were segregated into four groups. Group 1, control group; Group 2 received DIC-only; Groups 3, received CAR-only and group 4 received DIC plus CAR. Changes in biochemical indexes, pathological changes, molecular biological indexes, and genes related to the inflammation of main organs were evaluated. The results of this work indicated that the amounts of the serum protein carbonyl, sGOT, sGPT, urea, creatinine, uric acid, nitrite content, MDA, serum TNF-α, and renal TNF-α gene expression were remarkably increased and the levels of the GPx, GSH, CAT, and SOD were significantly reduced in DIC-only treated animals compared to the control group. On the other hand, treatment with CAR after exposure to DIC led to significant improvements in abnormalities of DIC-induced renal injury and serum biochemical factors. The data approve that CAR diminished the deleterious effects of DIC exposure. In this regard, the findings of this study indicated that the administration of CAR could alleviate the noxious effects of DIC on the antioxidant defense system and renal tissue.Ali NouriFarzad Izak-ShirianVahideh FanaeiMaryam DastanMahdieh AbolfathiAlireza MoradiMansoor KhalediHamzeh Mirshekari-JahangiriElsevierarticleCarvacrolDiclofenacOxidative stressDIC-induced renal injuryScience (General)Q1-390Social sciences (General)H1-99ENHeliyon, Vol 7, Iss 11, Pp e08358- (2021)
institution DOAJ
collection DOAJ
language EN
topic Carvacrol
Diclofenac
Oxidative stress
DIC-induced renal injury
Science (General)
Q1-390
Social sciences (General)
H1-99
spellingShingle Carvacrol
Diclofenac
Oxidative stress
DIC-induced renal injury
Science (General)
Q1-390
Social sciences (General)
H1-99
Ali Nouri
Farzad Izak-Shirian
Vahideh Fanaei
Maryam Dastan
Mahdieh Abolfathi
Alireza Moradi
Mansoor Khaledi
Hamzeh Mirshekari-Jahangiri
Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response
description Diclofenac (DIC) is an NSAID that can cause toxic effects in animals and humans and carvacrol (CAR) is a monoterpene compound that displays effective pharmacological and biological actions. The purpose of this work was to assess the influences of CAR on DIC-induced renal injury and oxidative stress in male rats. The rats were segregated into four groups. Group 1, control group; Group 2 received DIC-only; Groups 3, received CAR-only and group 4 received DIC plus CAR. Changes in biochemical indexes, pathological changes, molecular biological indexes, and genes related to the inflammation of main organs were evaluated. The results of this work indicated that the amounts of the serum protein carbonyl, sGOT, sGPT, urea, creatinine, uric acid, nitrite content, MDA, serum TNF-α, and renal TNF-α gene expression were remarkably increased and the levels of the GPx, GSH, CAT, and SOD were significantly reduced in DIC-only treated animals compared to the control group. On the other hand, treatment with CAR after exposure to DIC led to significant improvements in abnormalities of DIC-induced renal injury and serum biochemical factors. The data approve that CAR diminished the deleterious effects of DIC exposure. In this regard, the findings of this study indicated that the administration of CAR could alleviate the noxious effects of DIC on the antioxidant defense system and renal tissue.
format article
author Ali Nouri
Farzad Izak-Shirian
Vahideh Fanaei
Maryam Dastan
Mahdieh Abolfathi
Alireza Moradi
Mansoor Khaledi
Hamzeh Mirshekari-Jahangiri
author_facet Ali Nouri
Farzad Izak-Shirian
Vahideh Fanaei
Maryam Dastan
Mahdieh Abolfathi
Alireza Moradi
Mansoor Khaledi
Hamzeh Mirshekari-Jahangiri
author_sort Ali Nouri
title Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response
title_short Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response
title_full Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response
title_fullStr Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response
title_full_unstemmed Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response
title_sort carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response
publisher Elsevier
publishDate 2021
url https://doaj.org/article/b80a16b774f84adab6ab7caa39e9cd51
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