The role of Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways in mediating the protective effect of boric acid on acrylamide-induced acute liver injury in rats

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dc.authoridGUR, Fatma/0000-0001-5983-1472
dc.authoridCENGIZ, Mustafa/0000-0002-6925-8371
dc.authoridBAYRAKDAR, Alpaslan/0000-0001-7967-2245
dc.contributor.authorCengiz, Mustafa
dc.contributor.authorAyhanci, Adnan
dc.contributor.authorAkkemik, Ebru
dc.contributor.authorSahin, Ilknur Kulcanay
dc.contributor.authorGur, Fatma
dc.contributor.authorBayrakdar, Alpaslan
dc.contributor.authorCengiz, Betul Peker
dc.date.accessioned2024-12-24T19:27:28Z
dc.date.available2024-12-24T19:27:28Z
dc.date.issued2022
dc.departmentSiirt Üniversitesi
dc.description.abstractIntroduction: This study aims to investigate whether boric acid (BA) can protect rats from acrylamide (AA)induced acute liver injury. Materials and methods: AA was used to induce acute liver injury. Thirty rats were divided into five group including Group 1 (saline), Group 2 (AA), Group 3 (20 mg/kg BA), Group 4 (10 mg/kg BA+AA) and Group 5 (20 mg/kg BA+AA). Their blood and liver were harvested to be kept for analysis. Liver function enzyme activities were performed by spectrophotometric method. Catalase (CAT), superoxide dismutase (SOD) activity, and malondialdehyde levels were determined by colorimetric method. The in-silico studies were performed using the blind docking method. Results: Administration AA to rats, biochemical parameters, liver histology, and expression levels of apoptotic markers were negatively affected. However, after the administration of BA, the altered biochemical parameters, liver histology, and expression levels of apoptotic markers were reversed. Moreover, the mechanisms of AA-induced deterioration in the levels of SOD, CAT, and Nrf2-Keap-1 and the mechanisms of the protective effect of BA against these deteriorations were explained by in silico studies. Conclusion: Thus, the present study could explain the interactions between AA and thiol-containing amino acid residues of Keap-1, the effect of BA on these interactions, and the biochemical toxicity caused by the AA. In this sense, this work is the first of its kind in the literature. Based on the biochemical, histopathological, and in silico results, it can be suggested that BA has the potential to be used as a protective agent against AA-induced liver injury.
dc.description.sponsorshipSiirt University, Scientific Research Projects Unit [2021-S.IUE.GT-17]
dc.description.sponsorshipThe others would like to thank Siirt University, Scientific Research Projects Unit (2021-S.IUE.GT-17) for their support for our study.
dc.identifier.doi10.1016/j.lfs.2022.120864
dc.identifier.issn0024-3205
dc.identifier.issn1879-0631
dc.identifier.pmid35940215
dc.identifier.scopus2-s2.0-85135693682
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1016/j.lfs.2022.120864
dc.identifier.urihttps://hdl.handle.net/20.500.12604/6650
dc.identifier.volume307
dc.identifier.wosWOS:000858803200005
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherPergamon-Elsevier Science Ltd
dc.relation.ispartofLife Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241222
dc.subjectBiochemical toxicity
dc.subjectAcrylamide
dc.subjectBoric acid
dc.subjectMolecular modeling
dc.subjectLiver damage
dc.subjectRats
dc.titleThe role of Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways in mediating the protective effect of boric acid on acrylamide-induced acute liver injury in rats
dc.typeArticle

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