Oral pelargonidin exerts dose-dependent neuroprotection in 6-hydroxydopamine rat model of hemi-parkinsonism

Department of Physiology, School of Medicine, Shahed University and Medicinal Plant Research Center, Tehran, Iran.
Brain research bulletin (Impact Factor: 2.72). 07/2010; 82(5-6):279-83. DOI: 10.1016/j.brainresbull.2010.06.004
Source: PubMed


Parkinson's disease (PD) is a neuropathological and debilitating disorder involving the degeneration of mesencephalic dopaminergic neurons. Neuroprotective effect of pelargonidin (Pel) has already been reported, therefore, this study examined whether Pel administration would attenuate behavioural and structural abnormalities and markers of oxidative stress in an experimental model of PD in rat. For this purpose, unilateral intrastriatal 6-hydroxydopamine (6-OHDA, 12.5mug/5mul of saline-ascorbate)-lesioned rats were pre-treated p.o. with Pel (10 and/or 20mg/kg). Pel administration dose-dependently attenuated the rotational behavior in lesioned rats and protected the neurons of SNC against 6-OHDA toxicity. In addition, pre-treatment with Pel (20mg/kg) significantly decreased the 6-OHDA-induced thiobarbituric acid reactive substances (TBARS) formation, indicative of a neuroprotection against lipid peroxidation. Furthermore, the increase of nitrite levels induced by 6-OHDA, indicate the nitric oxide formation and free radicals production and the decrease of antioxidant defense enzyme superoxide dismutase (SOD) was non-significantly prevented by Pel (20mg/kg). In summary, Pel administration has a dose-dependent neuroprotective effect against 6-OHDA toxicity, partly through attenuating oxidative stress. Our findings suggest that pelargonidin could provide benefits, along with other therapies, in neurodegenerative disorders including PD.

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    • "After having the skull drilled carefully, single injection of 0.9 % saline containing 2.5 lg/ll of 6-hy- droxydopamine-HCl (6-OHDA, Sigma) and 0.2 % ascorbic acid (w/v) at a rate of 1 ll/min was injected through a 5 ll Hamilton syringe in anaesthetized rats. The act of injecting performed in a slow rate (1 ll/min) to minimize the possibility of damaging brain tissue [3]. The rats were placed equally in two groups mentioned before. "
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