الفهرس 
INTRODUCTION AND AIM OF THE WORK
PARKINSON’’S DISEASE ((PD))Only 14 pages are availabe for public view
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Abstract
This thesis is concerned with the evaluation of the neuroprotective potential of pramipexole and rasagiline in rotenone-treated mice. In addition, an attempt was undertaken to clarify the possible role of NO and oxidative stress in these effects.
Four groups of mice, 12 animals each, were used in this study. In the first group, experimental animals were treated with 4 ml/kg sunflower oil intraperitoneally once daily for 49 days. In the second group, animals received 2 mg/kg rotenone (dissolved in sunflower oil) IP once daily for 49 days. In the 3rd group, animals received pramipexole 1mg/kg IP dissolved in physiological saline at 1mg/1ml which was administered 30 min prior to rotenone (2 mg/kg/day; IP) for 49 days. In the 4th group, animals received rasagiline 1mg/kg IP dissolved in physiological saline at 1mg/ml and was administered 30 min prior to rotenone (2 mg/kg/day; IP) for 49 days.
Intraperitoneal administration of rotenone (2 mg/kg for 49 days) induced DA-ergic neuronal death which was associated with DA level decline and neurobehavioral deficit including loss of spontaneous locomotor activities, cataleptic behavior and depressant-like effect.
Pretreatment with pramipexole (1mg/kg, IP) or rasagiline (1mg/kg, IP) significantly inhibited the DA-ergic neuronal death induced by rotenone. These drugs also prevented the decline in the level of neurotransmitter DA as well as the behavioral manifestations of PD including loss of spontaneous locomotor activities, cataleptic behavior and depressant-like effect which were associated with chronic rotenone administration.
Chronic administration of rotenone produced decrease in total antioxidant capacity and increase in the Malondialdehyde production and NO level. Pretreatment with PPX or rasagiline (1 mg/kg, IP) prevented these biochemical changes.
In conclusions, both of pramipexole and rasagiline have neuroprotective effects against the dopaminergic neurodegeneration induced by the chronic intraperitoneal administration of rotenone not just a symptomatic therapy for PD. Pramipexole and rasagiline may produce these neuroprotective effects even in part through inhibition of rotenone induced oxidative stress and NO overproduction and through maintenance of the cellular antioxidant status. However, this thesis should be followed by further thorough experimental and clinical studies to elucidate precisely these mechanisms.