Author/Authors :
-، - نويسنده Pharmaceutical Research Center, Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran Mehri, Soghra , -، - نويسنده Pharmaceutical Research Center, Department of Medicinal Chemistry and Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran Abnous, Khalil , -، - نويسنده Department of Pathology, Imam Reza Hospital, School of Medicine, University of Medical Sciences, Mashhad, Iran Khooei, Alireza , -، - نويسنده Pharmacological Research Centre of Medicinal Plants; School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Mousavi, Seyed Hadi , -، - نويسنده Pharmacological Research Centre, Mashhad University of Medical Sciences, Mashhad, Iran Shariaty, Vahideh Motamed , -، - نويسنده Pharmaceutical Research Center, Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran Hosseinzadeh, Hossein
Abstract :
Objective(s):Acrylamide (ACR) has many applications in different industries. ACR damages the central and the peripheral nervous system in human and animals. Importance of ACR-induced neurotoxicity encouraged researchers to find both different mechanisms involved in ACR neurotoxicity and potent neuroprotective agents. Therefore, this study was designed to investigate the protective effect of crocin, an active constituent of Crocus sativus L. (saffron) on ACR-induced neurotoxicity in Wistar rats.
Materials and Methods: Animals were treated with ACR (50 mg/kg, IP) 11 days for induction neurotoxicity. Crocin (12.5, 25 and 50 mg/kg, IP) were used during treatment with ACR. At the end of treatment, gait score examination was performed. Then, rats were sacrificed and the severity of damage in brain tissue was determined using pathological tests. The level of malondialdehyde (MDA) and glutathione (GSH) content were evaluated in cerebral cortex and cerebellum to determine the role of oxidative stress in this model.
Results: Exposure to ACR induced severe gait abnormalities and pathological changes, but administration of crocin markedly improved behavioral index and histopathological damages. The elevation of lipid peroxidation parallel with reduction of GSH level was observed in cerebral cortex and cerebellum following exposure to ACR. Treatment with crocin markedly decreased MDA level, while elevated GSH content in nervous system as compared to ACR-treated animals.
Conclusion: The administration of crocin markedly improved behavioral and histopathological damages in Wistar rats exposed to ACR. Reduction of oxidative stress can be considered as an important mechanism of neuroprotective effects of crocin against ACR-induced toxicity.
