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RESEARCH ARTICLE
Year : 2018  |  Volume : 7  |  Issue : 3  |  Page : 344-356

Protective effect of grape seed extract against acrylamide-induced neurotoxicity in Vitro and In Vivo


1 Department of Pharmacodynamics and Toxicology, 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; Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

Correspondence Address:
Hossein Hosseinzadeh
Department of Pharmacodynamics and Toxicology, School of Pharmacy; Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad
Iran
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Source of Support: None, Conflict of Interest: None


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Acrylamide (ACR) monomer is an effective neurotoxicant, which damages the central and peripheral nervous systems in humans and animals. It also has broad applications in different industries. Grape seed extract (GSE) possesses antioxidant properties. The present study was designed to evaluate the beneficial effects of GSE against ACR-induced neurotoxicity in both in vitro and in vivo. In our in vitro study, the effect of different concentrations of GSE on ACR toxicity (IC50) in PC12 cells was evaluated using MTT assay. Moreover, in another experiment, the effect of GSE on neural toxicity induced by ACR was evaluated in rats. Pretreatment with GSE (10-100 μM) significantly decreased ACR induced cytotoxicity. In Wistar rats, exposure to ACR (50 mg/kg IP for 11days), significantly induced severe gait abnormalities but treatment with GSE (12.5 mg/kg) reduced ACR induced neurotoxicity in animals. After that, rats were sacrificed and malondialdehyde (MDA) as a marker of lipid peroxidation and GSH content were determined in brain tissue. ACR induced lipid peroxidation and increased level of MDA, while reduced GSH level. Treatment with GSE significantly reduced level of MDA and increased GSH content in cerebral cortex (p<0.001). The results suggest that the neuroprotective effect of GSE in this model in part, may be due to its ability to scavenge free radicals and its effective recovery of the antioxidative defense system.


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