Document Type : Original Research Article
Authors
1
School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
2
Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
3
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
10.22038/ajp.2024.24950
Abstract
Objective: The Maillard reaction generates acrylamide (ACR), a toxic compound commonly found in laboratory and industrial settings. ACR exposure, both short-term and long-term, can damage various organs, notably the central nervous system, through oxidative stress, inflammation, and apoptosis. This study explores the potential neuroprotective effects of zeaxanthin (ZEA), known for its antioxidant, anti-inflammatory, and anti-apoptotic properties, against ACR-induced toxicity in the rat cerebral cortex.
Materials and Methods: Rats were subjected to ACR exposure (50 mg/kg, intraperitoneal injection) for 11 days and subsequently, treated with ZEA (20-80 mg/kg, intragastric gavage) for either 11 or 20 days to assess both preventive and therapeutic effects. Locomotor behavior was evaluated using a gait score test, while biochemical analyses measured malondialdehyde (MDA) and glutathione (GSH) levels, inflammatory markers interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α), and apoptotic markers (cleaved caspase-3) in the cerebral cortex.
Results: ACR exposure impaired locomotion in the animals, but ZEA treatment significantly improved gait scores when administered preventatively (from days 6-11) or therapeutically (from days 6-20). ACR also led to increased MDA levels and depleted GSH content in brain tissue, and it elevated IL-1β, TNF-α, and cleaved caspase-3 in the cerebral cortex. However, ZEA supplementation, along with vitamin E, effectively reversed these alterations compared to the ACR-exposed group.
Conclusion: In conclusion, ZEA demonstrates both preventive and therapeutic effects against ACR-induced neurotoxicity. These findings suggest that ZEA could serve as an effective preventive agent by countering ACR-induced damage through its antioxidant, anti-inflammatory, and anti-apoptotic mechanisms.
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