Carvacrol prevents acrylamide-induced oxidative and inflammatory liver damage and dysfunction in rats

ArticleAçık Erişim

Özet

Background: Acrylamide causes hepatotoxicity with the effect of oxidative stress and inflammatory processes. Carvacrol is a monoterpenic phenol with antioxidant and anti-inflammatory properties. Aims: To determine the effects of carvacrol on oxidative liver injury induced by acrylamide administration in rats. Methods: Rats were divided into three groups of six animals each: healthy group acrylamide group (ACR), and acrylamide + carvacrol group (TACR). First, carvacrol (50 mg/kg) was administered intraperitoneally to the CACR group. One hour later, acrylamide (20 mg/kg) was given orally to the ACR and CACR groups. This procedure was performed for 30 days, after which the animals were sacrificed. The malondialdehyde (MDA) and total glutathione (tGSH) levels, total oxidant (TOS) and total antioxidant status (TAS), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and nuclear factor kappa b (NF-κB) were measured in the excised liver tissues. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were determined in blood serum samples. Liver tissues were also examined histopathologically. Results: In the ACR group, malondialdehyde, TOS, ALT, AST levels, and NF-κB, IL-1β, and TNF-α levels were found to be high, and tGSH and total antioxidant status levels were low. In addition, diffuse degenerative changes and necrosis in hepatocytes, and moderate inflammation in the portal region were detected in the liver tissues of the ACR group. While carvacrol prevented the biochemical changes induced by acrylamide, it also alleviated the damage in the histological structure. Conclusion: Carvacrol may be used for liver damage caused by acrylamide. Copyright © 2023 Cerrah, Ozcicek, Gundogdu, Cicek, Coban, Suleyman, Altuner, Bulut and Suleyman.

Anahtar Kelimeler

RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/12385Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.3389/fphar.2023.1161448Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorCerrah, Serkan
dc.contributor.authorOzcicek, Fatih
dc.contributor.authorGundogdu, Betul
dc.contributor.authorCicek, Betul
dc.contributor.authorCoban, Taha Abdulkadir
dc.contributor.authorSuleyman, Bahadir
dc.contributor.authorAltuner, Durdu
dc.contributor.authorBulut, Seval
dc.contributor.authorSuleyman, Halis
dc.date.accessioned2026-10-18T20:27:17.717481032Z
dc.date.available2026-10-18T20:27:17.717481032Z
dc.date.issued2023
dc.description.abstractBackground: Acrylamide causes hepatotoxicity with the effect of oxidative stress and inflammatory processes. Carvacrol is a monoterpenic phenol with antioxidant and anti-inflammatory properties. Aims: To determine the effects of carvacrol on oxidative liver injury induced by acrylamide administration in rats. Methods: Rats were divided into three groups of six animals each: healthy group acrylamide group (ACR), and acrylamide + carvacrol group (TACR). First, carvacrol (50 mg/kg) was administered intraperitoneally to the CACR group. One hour later, acrylamide (20 mg/kg) was given orally to the ACR and CACR groups. This procedure was performed for 30 days, after which the animals were sacrificed. The malondialdehyde (MDA) and total glutathione (tGSH) levels, total oxidant (TOS) and total antioxidant status (TAS), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and nuclear factor kappa b (NF-κB) were measured in the excised liver tissues. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were determined in blood serum samples. Liver tissues were also examined histopathologically. Results: In the ACR group, malondialdehyde, TOS, ALT, AST levels, and NF-κB, IL-1β, and TNF-α levels were found to be high, and tGSH and total antioxidant status levels were low. In addition, diffuse degenerative changes and necrosis in hepatocytes, and moderate inflammation in the portal region were detected in the liver tissues of the ACR group. While carvacrol prevented the biochemical changes induced by acrylamide, it also alleviated the damage in the histological structure. Conclusion: Carvacrol may be used for liver damage caused by acrylamide. Copyright © 2023 Cerrah, Ozcicek, Gundogdu, Cicek, Coban, Suleyman, Altuner, Bulut and Suleyman.
dc.identifier.doi10.3389/fphar.2023.1161448
dc.identifier.eissn1663-9812
dc.identifier.issn1663-9812
dc.identifier.pmcidPMC10113504
dc.identifier.pmid37089925
dc.identifier.scopus2-s2.0-85153048007
dc.identifier.startpage1161448
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/12385
dc.identifier.volume14
dc.identifier.wosWOS:000974656100001
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.relation.ispartofFrontiers in Pharmacology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectacrylamide
dc.subjectcarvacrol
dc.subjectexperimental models
dc.subjectliver damage
dc.subjectoxidative stress
dc.subjectalanine aminotransferase
dc.subjectaspartate aminotransferase
dc.subjectglutathione
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinterleukin 1beta
dc.subjectmalonaldehyde
dc.subjecttumor necrosis factor
dc.subjectalanine aminotransferase blood level
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectantioxidant activity
dc.subjectArticle
dc.subjectaspartate aminotransferase blood level
dc.subjectbiochemical analysis
dc.subjectcontrolled study
dc.subjectdrug mechanism
dc.subjectexperimental model
dc.subjectgene expression
dc.subjecthistopathology
dc.subjectinflammation
dc.subjectliver cell
dc.subjectliver disease
dc.subjectliver dysfunction
dc.titleCarvacrol prevents acrylamide-induced oxidative and inflammatory liver damage and dysfunction in rats
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus35
rdl.citation.wos30
rdl.departmentDepartment of Internal Medicine, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Türkiye. | Department of Physiology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Türkiye. | Department of Clinical Biochemistry, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Türkiye. | Department of Pharmacology, Faculty of Medicine, Erzincan Binali Yildirim University, Erzincan, Türkiye.
rdl.oa.statusgold
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)