Mashhad Razavi Hospital Razavi Journal of Medicine 3115-753X 14 2 2026 04 01 Neuroprotective Effects of Morin Against Acrylamide-Induced Cytotoxicity in PC12 Cells 12 23 118618 10.30483/rjm.2026.254683.1453 EN Shabnam Shahsavand Department of Medicine, North Khorasan University of Medical Sciences, Bojnurd, Iran Simin Joharinia North Khorasan University of Medical Sciences, Bojnurd, Iran Iraj Javadi Department of Toxicology, Shahreza Branch, Islamic Azad University, Shahreza, Iran 0000-0002-9697-2343 Reza Ghasemi Department of Cardiology, School of Medicine, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran 0000-0002-0846-7292 Atefeh Shirinzadeh Feizabadi Department of Anesthesiology, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran Journal Article 2025 10 20 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 PC12 cells. Methods: PC12 cells were pretreated with various concentrations of morin (25–400 µM) for 24 hours, followed by exposure to ACR (4.5 mM, IC₅₀ value) for another 24 hours. Cell viability was assessed by MTT assay. Apoptosis was evaluated by flow cytometry using the Sub-G1 peak method, and intracellular reactive oxygen species (ROS) levels were measured using DCF-DA. Results: ACR induced cytotoxicity in a concentration-dependent manner (IC₅₀ = 4.5 mM) and significantly increased both apoptotic cell percentage (to 21.25 ± 1.32%; p < 0.001) and ROS levels (p < 0.001) compared to control. Pretreatment with morin significantly attenuated ACR-induced cytotoxicity in a concentration-dependent manner (p < 0.001), reduced apoptosis (to 5.17 ± 0.86%; p < 0.001), and decreased ROS production (p < 0.001). Morin alone showed no cytotoxicity and reduced basal ROS levels (p < 0.001). 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.

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