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

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 (۳۸.۲۷ mg/kg) and morin (۵۰ or ۱۰۰ 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 ۲-related factor ۲ (Nrf-۲), heme oxygenase-۱ (HO-۱), NAD(P)H dehydrogenase quinone ۱ (NQO۱), 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-۲ (Bcl-۲) associated X protein (Bax), caspase-۳, and apoptotic peptidase activating factor ۱ (apaf-۱) expressions, elevated by ACR in the heart tissue, were suppressed after morin administration. Moreover, Bcl-۲ 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.

کلیدواژه ها:

Apoptosis ، Acrylamide ، Cardiotoxicity ، Endoplasmic reticulum- stress ، Morin