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ORIGINAL ARTICLE
Year : 2018  |  Volume : 8  |  Issue : 2  |  Page : 47-52

Oxidative Stress Status and Neuroprotection of Tocotrienols in Chronic Cerebral Hypoperfusion-Induced Neurodegeneration Rat Animal Model


1 Department of Basic Medical Sciences, Faculty of Medicine, International Islamic University Malaysia (IIUM), Kuantan, Pahang, Malaysia; Department of Clinical Pharmacology, Menoufia Medical School, Menoufia University, Menoufia, Egypt
2 Department of Basic Medical Sciences, Faculty of Medicine, International Islamic University Malaysia (IIUM), Kuantan, Pahang, Malaysia

Correspondence Address:
Wael M.Y Mohamed
Department of Basic Medical Sciences, Faculty of Medicine, International Islamic University Malaysia (IIUM), Kuantan, Pahang, Malaysia; Department of Clinical Pharmacology, Menoufia Medical School, Menoufia University, Menoufia, Egypt

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijnpnd.ijnpnd_17_18

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Background: Reduced cerebral blood flow is associated with aging, neurodegenerative disorders, and an increased formation of reactive oxygen species. This study was designed to assess the potential use of vitamin E as an antioxidant and neuroprotective agent using 2-vessel occlusion (2VO) rat animal model. Materials and Methods: Twenty-four Sprague Dawley rats weighing 200–250 g were equally divided into the following three groups: SHAM control, 2VO, and 2VO+E (treated daily with vitamin E tocotrienol, 100 mg/kg, orally following 2VO). On the 8th week after 2VO surgery, rats were euthanized and the hippocampi were isolated with the estimation of viable neuronal cell count in the hippocampal CA-1 region. The isoprostane F2 (Iso-F2) levels were also measured in the brain homogenates to quantify the oxidative stress levels. Results: There was significantly higher neuronal cell death in the hippocampal CA-1 region and increased Iso-F2 levels in the 2VO group compared to the SHAM control group (P < 0.05). Conversely, no significant difference was observed with regard to the neuronal cell death and Iso-F2 levels in the 2VO+E group and the SHAM control group (P > 0.05). Conclusion: This study demonstrates the effectiveness of vitamin E tocotrienol as a neuroprotective and antioxidant agent in chronic cerebral hypoperfusion-induced neurodegeneration in rats.


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