مرکز منطقه ای اطلاع رساني علوم و فناوري -

چكيده لاتين :

Free radical formation and oxidative stress might play an important role in the pathogenesis of Parkinsonיs disease (PO ). In vitro data indicate that neuromelanin (NM) pigment is formed the excess cytosolic catecholamine that is not accumulated into synaptic vesicles via the vesicular monoamine transporter 2 (VMAT2). We designed this study to inve stigate the neuroprotective effects of vitamin E in the early model of PD. Methods: Male rats (n = 40) with unb iased rotational behav ior were randomly divided into five groups: sham operated group (SH , n = 8), vehicle-treated SH group (SH + V, n = 8), vitamin E-treated SH group (SH + E, n = 8), vehicle-treated lesion group (L + V, n = 8) and vitamin E-treated lesion group (L + E, n = 8). Unilateral intrastriatal 6-hydroxydopamine (12 .5 Ill) lesioned rats were treated intramuscularly with utocopherol acid succinate (24 I.U/kg, intramuscular [i.m.]) I h before surgery and three times per week for 2 month post-surgery. To evaluate the vitamin E pretreatment efficacy, tyrosine hydroxylase (TH) immunoreactivity and immunostaining intensity (lSI) for monoamine transporter 2 were used. Results: TH immunohistochemical analyses showed a redu ct ion of 20% in locu s coeruleus (LC) cell number of vitamin E pretreated lesioned group but the cell number dropped to 60% in the lesioned group. The lSI of the cells was measured for VMAT2 in LC. Lesioned groups : I) had the lowest VMAT2 lSI of all neurons; 2) There was an inverse relationship between VMAT2 lSI and NM pigment in the locus and 3) Neurons with the highest VMAT2 lSI also had high TH lSI. Conclusion: The data support the hypothesis that repeated i.m. administration of vitamin E exerts a protective effect on the LC neurons in the earl y model of PD. fran. Biomed. J 12 (4): 217-222, 2008