Razavi Journal of Medicine

Razavi Journal of Medicine

Neuroprotective Effects of Morin Against Acrylamide-Induced Cytotoxicity in PC12 Cells

Document Type : Original Article

Authors
1 Department of Medicine, North Khorasan University of Medical Sciences, Bojnurd, Iran
2 North Khorasan University of Medical Sciences, Bojnurd, Iran
3 Department of Toxicology, Shahreza Branch, Islamic Azad University, Shahreza, Iran
4 Department of Cardiology, School of Medicine, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran
5 Department of Anesthesiology, Torbat Heydariyeh University of Medical Sciences, Torbat Heydariyeh, Iran
Abstract
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.
Keywords

Acknowledgements: Authors gratefully acknowledge Dr. Soghra Mehri for her generous advice that greatly enhanced the manuscript.

 

Availability of data and materials: The data that support the findings of this study are available within the article and its supplementary materials. Further inquiries can be directed to the corresponding author.

 

Conflicts of interests: The author declares that there are no conflicts of interest.

 

Consent for publication: Not applicable.

 

Ethics approval and consent to participate: Not applicable.

 

Financial disclosure: This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

 

Author contributions: Sh.Sh.: Contributed to the conception of the work, revising the draft, approving the final version of the manuscript, and agreeing on all aspects of the work; S. J.: Contributed to the conception and design of the study, drafting of the manuscript and critical revision, and approval of final version I.J., R.Gh, and A.Sh.F.: Contributed to the conception and design of the study, critical revision, and approval of the manuscript's final version.

 

Open Access Policy: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. To view a copy of this licence, visit https://creativecommons.org/licenses/by/4.0/

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