Journal
NEUROCHEMICAL RESEARCH
Volume 37, Issue 3, Pages 516-526Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-011-0638-4
Keywords
Sesame seed oil (SO); Parkinson disease (PD); Neurotoxicity; NADPH oxidase; Antioxidants; Tyrosine hydroxylase
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Funding
- Department of Science and Technology (DST), New Delhi, Govt. of India
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Natural antioxidants have shown a remarkable reduction in oxidative stress due to excess formation of reactive oxygen species by enhancing antioxidant mechanism in the neurodegenerative disorders. Sesame seed oil (SO) is one of the most important edible oil in India as well as in Asian countries and has potent antioxidant properties thus the present study evaluated the neuroprotective effect of SO by using 6-Hydroxydopamine (6-OHDA)-induced Parkinson's disease model in mice. The mice were fed an SO mix diet for 15 days and then 6-OHDA was injected into the right striatum of mice brain. Three weeks after 6-OHDA infusion, mice were sacrificed and the striatum was removed. The neuroprotective role of SO on the activities of antioxidant and non-antioxidant enzymes such as glutathione reductase (GR), glutathione-S-transferase (GST), glutathione peroxidase (GPx), catalase (CAT) and content of glutathione (GSH) and thiobarbituric acid reactive substance (TBARS) were studied in the striatum. The activities of all the above-mentioned enzymes decreased significantly in 6-OHDA group (Lesioned) when compared with Sham. The pretreatment of SO on antioxidant mechanism and dopamine level in the brain had shown some significant improvement in Lesion+SO (L+SO) group when compared with Lesioned group. However, NADPH oxidase subunit, Nox2 and inflammatory stimulator Cox2 expression was increased as well as antioxidant MnSOD level was decreased in Lesioned group while SO showed the inhibitory effect on the activation of Nox2 and Cox2 and restored MnSOD expression in L+SO group. Increased tyrosine hydroxylase (TH) expression in substantia nigra as well as dopamine and its metabolite DOPAC level in L+SO group also support our findings that SO may inhibit activation of NADPH oxidase dependent inflammatory mechanism due to 6-OHDA induced neurotoxicity in mice.
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