Neuroprotective effect of vitamin E on the early model of Parkinson's disease in rat: behavioral and histochemical evidence

Alternative Medicine Review, April, 2001 by M Roghani, G. Behzadi

There is strong evidence that oxidative stress participates in the etiology of Parkinson's disease (PD). We designed this study to investigate the neuroprotective effect of vitamin E in the early model of PD. For this purpose, unilateral intrastriatal 6-hydroxydopamine (12.5 ?g/5 ?1) lesioned rats were pretreated intramuscularly with D-alpha-tocopheryl acid succinate (24 I.U./ kg, i.m.) 1 h before and three times per week for 1 month post-surgery. Apomorphine- and amphetamine-induced rotational behavior was measured postlesion fortnightly. A parallel tyrosine hydroxylase immunoreactivity and wheat germ agglutinin-horse radish peroxidase (WGA-HRP) tract-tracing study was performed to evaluate the vitamin E pretreatment efficacy. Tyrosine hydroxylase-immunohistochemical analyses showed a reduction of 18% in ipsilateral substantia nigra pars compacta (SNC) cell number of the vitamin E-pretreated lesioned (L E) group comparing with contralateral side. The cell number dropped to 53% in the lesioned (L V) group. In addition, retrograde-labeled neurons in ipsilateral SNC were reduced by up to 30% in the L E group and 65% in the L V group. Behavioral tests revealed that there are 74% and 68% reductions in contraversive and ipsiversive rotations in the L E group, respectively, as compared with the L V group. Therefore repeated intramuscular administration of vitamin E exerts a rapid protective effect on the nigrostriatal dopaminergic neurons in the early unilateral model of PD.

Roghani M, Behzadi G, Brain Res 2001;892:211-217.

COPYRIGHT 2001 Thorne Research Inc.
COPYRIGHT 2001 Gale Group
 

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