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
نویسندگان
1 İstanbul Atlas University, Faculty of Medicine, Department of Emergency Medicine, İstanbul, Turkey
2 Atatürk University, Vocational School of Health Services, Department of Medical Laboratory Techniques, Erzurum, Turkey
3 Atatürk University, Horasan Vocational College, Department of Animal Science, Erzurum, Turkey
4 Atatürk University, Faculty of Veterinary Medicine, Department of Biochemistry, Erzurum, Turkey
5 Aksaray University, Faculty of Medicine, Department of Cardiology, Aksaray, Turkey
6 Final Inernational University, Vocational School of Health Services, Cyprus, Turkey
doi
10.22038/ijbms.2024.81490.17634چکیده
Objective(s): The present study investigated whether morin has a protective effect against ACR-induced 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.
