:: Volume 18, Issue 2 (4-2014) ::
IBJ 2014, 18(2): 101-106 Back to browse issues page
Chrysin Reduced Acrylamide-Induced Neurotoxicity in Both in vitro and in vivo Assessments
Soghra Mehri , Hamed Veis Karami , Faezeh Vahdati Hassani , Hossein Hosseinzadeh
Abstract:  
Background: Acrylamide (ACR) is a well-known industrial toxic chemical that produces neurotoxicity, which is characterized by progressive central and peripheral neuronal degeneration. Chrysin is a natural, biologically active flavonoid compound, which is commonly found in many plants. The antioxidant and neuroprotective properties of chrysin have been demonstrated. Methods: In this study, the possible effect of chrysin on ACR-induced toxicity was evaluated in both in vitro and in vivo experiments. PC12 cells were used as a suitable in vitro model. Cells were exposed to chrysin (0.5-5 µM) for 12 and 24 h, and then ACR in IC50 concentration was added to the cells. Finally, cell viability was determined using (4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium assay. For in vivo assay, Wistar rats were treated with ACR (50 mg/kg i.p. for 11 days) alone or in combination with chrysin (12.5, 25, and 50 mg/kg). At the end of treatment, behavioral index was evaluated. Results: ACR decreased cell viability and pre-treatment with chrysin (0.5-5 µM) significantly decreased ACR-induced cytotoxicity in the time- and dose-dependent manner. In Wistar rats, exposure to ACR significantly induced severe gait abnormalities, but treatment with chrysin (50 mg/kg) reduced ACR-induced neurotoxicity in animals. Conclusion: In the current study, chrysin exhibited neuroprotective effect on PC12 cells as an in vitro model and also on Wistar rats.
Keywords: Acrylamide, Chrysin, Neurotoxicity, Antioxidant
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Type of Study: Full Length | Subject: Related Fields
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Mehri S, Veis Karami H, Vahdati Hassani F, Hosseinzadeh H. Chrysin Reduced Acrylamide-Induced Neurotoxicity in Both in vitro and in vivo Assessments. IBJ. 2014; 18 (2) :101-106
URL: http://ibj.pasteur.ac.ir/article-1-1134-en.html


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