Cardiotoxicity caused by acrylamide in rats can be alleviated as a result of suppression of oxidative stress, endoplasmic reticulum stress, inflammation, and apoptosis by morin treatment

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dc.authorid0000-0002-5770-3554
dc.authorid0000-0002-8222-5515
dc.authorid0000-0001-6775-7858
dc.authorid0000-0002-4581-4492
dc.contributor.authorÇakmak, Fatma
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorGür, Cihan
dc.contributor.authorİleritürk, Mustafa
dc.contributor.authorGül, Murat
dc.contributor.authorVarışlı, Behçet
dc.date.accessioned2025-07-14T06:49:45Z
dc.date.available2025-07-14T06:49:45Z
dc.date.issued2025
dc.departmentTıp Fakültesi
dc.description.abstractThe present study investigated whether morin has a protective effect against ACRinduced cardiac toxicity. Materials and Methods: In this study, oxidative stress, inflammation, endoplasmic reticulum stress (ERS), and apoptosis markers in heart tissues were analyzed by different methods after ACR (38.27 mg/kg) and morin (50 or 100 mg/kg) oral administration for ten days to Sprague Dawley rats. Results: The data obtained showed that ACR induced lipid peroxidation by decreasing superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) enzyme activities, glutathione (GSH) levels and nuclear factor erythroid 2-related factor 2 (Nrf-2), heme oxygenase-1 (HO-1), NAD(P)H dehydrogenase quinone 1 (NQO1), glutamate-cysteine ligase modifier subunit (GCLM), and glutamate-cysteine ligase catalytic subunit (GCLC) gene expressions. On the other hand, these markers approached the control group levels after morin treatment. Moreover, morin suppressed ACR-induced inflammatory genes. Morin down-regulated the related genes by reducing the ERS, exacerbated after ACR administration. In addition, it was observed that B-cell lymphoma-2 (Bcl-2) associated X protein (Bax), caspase-3, and apoptotic peptidase activating factor 1 (apaf-1) expressions, elevated by ACR in the heart tissue, were suppressed after morin administration. Moreover, Bcl-2 expression was triggered by morin treatment. Thus, morin suppressed ACR-induced apoptosis. Conclusion: Taken together, morin may protect against ACR-induced cardiac injury by suppressing oxidative stress, inflammation, ERS, and apoptosis.
dc.identifier.doi10.22038/ijbms.2024.81490.17634
dc.identifier.endpage84
dc.identifier.issn20083866
dc.identifier.issue3
dc.identifier.scopus85214826645
dc.identifier.startpage76
dc.identifier.urihttps://dx.doi.org/10.22038/ijbms.2024.81490.17634
dc.identifier.urihttps://hdl.handle.net/20.500.12451/13283
dc.identifier.volume28
dc.identifier.wosWOS:001412925300013
dc.identifier.wosqualityQ3
dc.indekslendigikaynakScopus
dc.indekslendigikaynakWeb of Science
dc.institutionauthorGül, Murat
dc.language.isoen
dc.publisherMashhad University of Medical Sciences
dc.relation.ispartofIranian Journal of Basic Medical Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAcrylamide
dc.subjectApoptosis
dc.subjectCardiotoxicity
dc.subjectEndoplasmic Reticulum -stress
dc.subjectMorin
dc.titleCardiotoxicity caused by acrylamide in rats can be alleviated as a result of suppression of oxidative stress, endoplasmic reticulum stress, inflammation, and apoptosis by morin treatment
dc.typeArticle

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