الفهرس 
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Abstract
The aim of the present work was to study the possible neuroprotective effect of the nootropic drugs, piracetam and vincamine, in haloperidol-induced Parkinson’s disease in male rats, as well as, to study some of their possible underlying mechanisms, and whether their combination provides a better protection or not.
To achieve this aim, sixty-four adult male Wister albino rats were used. Rats were equally divided into eight experimental groups: control, piracetam-treated control, vincamine-treated control, combined piracetam and vincamine-treated control, haloperidol-induced Parkinson’s disease, piracetam-treated haloperidol-induced Parkinson’s disease, vincamine-treated haloperidol-induced Parkinson’s disease and combined piracetam and vincamine-treated haloperidol-induced Parkinson’s disease.
After 4 weeks-experimental period, neurological tests including Y-maze, stepping test, forced swimming test and olfactory preferring test were done to assess motor function and for cognitive and behavioral evaluation. Then, fasting blood samples were collected, left to clot, and then centrifuged and the serum was collected and stored at -20˚C until used for estimation of serum glucose, calcium, CPK and GDNF levels. Immediately after sacrification of rats, they were decapitated, and brains were carefully dissected. The basal ganglia of left hemispheres were isolated, and the striatal tissue was homogenized using glass rod. The homogenate was centrifuged, and the supernatant was kept at -80°C until used for estimation of dopamine, MDA, nitrite/nitrate, TNF-α, IL-1ß and GSH levels, and GPX and SOD activities. The right hemispheres were preserved in 10% formalin to be used for histopathological studies.
In the present study, non-significant differences in all the measured parameters were observed between control, piracetam-treated control, vincamine-treated control and combined piracetam and vincamine-treated control groups of rats.
The haloperidol-induced PD group showed significant reduction in number of adjusting steps of stepping test, percentage of alternation of Y-maze, duration of olfaction, latency to immobility of swimming test, serum calcium level, serum GDNF level, striatal dopamine level and striatal GSH levels, and the GPX and SOD activities, when compared with the corresponding values of the control group. Significant increases in immobility time of swimming test, serum glucose, serum CPK, striatal MDA, nitrite/nitrate, TNF-α and IL-1ß levels were observed in PD group versus control one. The histopathological findings of Basal ganglia in PD group showed decreased dopaminergic neurons and neuronal degeneration, inflammation, extensive hemorrhage and congested blood vessels, and numerous Lewis bodies, which were not seen in the normal structural appearance in control group.