Çakmak, FatmaKüçükler, SefaGür, Cihanİleritürk, MustafaGül, MuratVarışlı, Behçet2025-07-142025-07-14202520083866https://dx.doi.org/10.22038/ijbms.2024.81490.17634https://hdl.handle.net/20.500.12451/13283The 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.eninfo:eu-repo/semantics/openAccessAcrylamideApoptosisCardiotoxicityEndoplasmic Reticulum -stressMorinArticle283768410.22038/ijbms.2024.81490.1763485214826645WOS:001412925300013Q3