Neuroprotective Effects of Morin Against Acrylamide-Induced Cytotoxicity in PC۱۲ Cells

Background: Acrylamide (ACR) is widely used in industry and is also formed in carbohydrate-rich foods during high-temperature cooking processes. The neurotoxicity of ACR in humans and animals is well established, and multiple mechanisms have been proposed to mediate its toxic effects. Among these, oxidative stress and apoptosis pathways have gained considerable attention in recent years. Morin, a bioactive flavonoid found in mulberry, has demonstrated neuroprotective properties, particularly due to its antioxidant and anti-apoptotic activities. Objective: The present study aimed to evaluate ACR-induced neurotoxicity and the potential protective effects of morin in an in vitro model using PC۱۲ cells. Methods: PC۱۲ cells were pretreated with various concentrations of morin (۲۵–۴۰۰ µM) for ۲۴ hours, followed by exposure to ACR (۴.۵ mM, IC₅₀ value) for another ۲۴ hours. Cell viability was assessed by MTT assay. Apoptosis was evaluated by flow cytometry using the Sub-G۱ peak method, and intracellular reactive oxygen species (ROS) levels were measured using DCF-DA. Results: ACR induced cytotoxicity in a concentration-dependent manner (IC₅₀ = ۴.۵ mM) and significantly increased both apoptotic cell percentage (to ۲۱.۲۵ ± ۱.۳۲%; p < ۰.۰۰۱) and ROS levels (p < ۰.۰۰۱) compared to control. Pretreatment with morin significantly attenuated ACR-induced cytotoxicity in a concentration-dependent manner (p < ۰.۰۰۱), reduced apoptosis (to ۵.۱۷ ± ۰.۸۶%; p < ۰.۰۰۱), and decreased ROS production (p < ۰.۰۰۱). Morin alone showed no cytotoxicity and reduced basal ROS levels (p < ۰.۰۰۱). Conclusion: Oxidative stress and apoptosis play key roles in ACR-induced neurotoxicity. Morin exerts neuroprotective effects by reducing intracellular ROS production and, consequently, lowering apoptosis levels, thereby significantly mitigating ACR-induced neuronal damage.

کلیدواژه ها:

Acrylamide ، Morin ، oxidative stress ، Apoptosis