الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Parkinson’s disease is the second most common neurodegenerative disease after Alzheimer’s disease. It affects mainly the motor system due to the strongly degeneration of dopaminergic cells in the SN, a region of the midbrain. It is characterized by slowness of movement, rigidity, shaking, difficulty with walking and some psychiatric problems like depression. The current treatments can provide a cure in early stages of the disease but not in advances stages. The scientists are going to solve this problem by finding different drugs that has neuroprotective effect and hence have the ability to protect against PD. The present study was undertaken to evaluate the potential neuroprotective effect of two selected therapeutic agents: tiron and nebivolol. Mouse model using MPTP has been selected because it mimics many aspects of the disease which owes in humans. It is an important tools for understanding PD. This model is important as it illustrate PD symptoms and signs in human. It was used to achieve such results through inducing hypoactivity in open field test, increasing immobility time in forced swimming test, increasing MDA level and decreasing catalase, DA, GABA and Nrf2 levels and also through worsening histopathological and immunohistochemical states. Tiron might be beneficial as a neuroprotective agent because of its antioxidant and behavioural modulatory ability. It increases antioxidant markers and dopamine level significantly and reduces oxidative stress. It improve behavioural, histopathological and immunohistochemical states. Nebivolol might have an important role in neurodegenerative disorders. It increases antioxidant markers and dopamine level significantly and reduces oxidative stress. It improve behavioural, histopathological and immunohistochemical states. In conclusion, the present study demonstrated that treatment with either tiron or nebivolol at different doses in mice induced gradual improvement in both behavioral and biochemical alterations in most measured parameters. Both tiron and nebivolol conferred a neuroprotective role against the MPTP-induced parkinsonian mouse model. It was obvious in our study that higher dose of tiron gave better results in comparison with lower dose in the majority of parameters. Also, nebivolol higher dose seemed to be preferred. This neuroprotective impact could be attributed to its strong antioxidant ability through activating Keap-1/Nrf-2 pathway besides direct hydroxyl radical and superoxide scavenging capacity. Further clinical investigations might be required to assure these effects and study the applicability of the usage of tiron and nebivolol in management of PD.