Parkinson Hastalığının MPP+ Sıçan Modelinde Mezensefalon ve Önerilen İnteraktomda Proteomik Profil: Simvastatin Rolü

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Parkinson’s disease is a neurodegenerative disorder characterized by oxidative stress and immune activation in the nigro-striatal pathway. Simvastatin regulates cholesterol me-tabolism and protects from atherosclerosis. Parkinson´s disease neurological symptoms are caused by the loss of dopamine-producing cells in the midbrain, which results in mo-tor function deterioration. Simvastatin-tween 80/ DOSIS day was administered 7 days be-fore stereotaxic intrastriatal administration of 1-methyl-4-phenylpyridine (MPP+) in rats. Fluorescent lipidic product formation, dopamine levels, and circling behavior were evalu-ated as damage markers. Twenty-four hours and six days after MPP+ lesion, rats showed significant damage in relation to the control group. Simvastatin significantly reduced the MPP+-induced damage as compared to the MPP+ lesioned group. Apoptosis promotes neuroinflammation and neuronal degeneration in Parkinson’s disease; we search for rat protein homologs related to the inflammation response. We found that most proteins re-lated to neuroinflammation in the ventral midbrain decreased in the simvastatin-treated rats. Furthermore, differential expression of antioxidant enzymes in mesencephalic tissue of rat brains was found in response to simvastatin. These results suggest that simvastatin could prevent MPP+-induced damage in the nigrostriatal pathway and, for the first time, suggest that the molecular mechanisms involved in this protective effect occur through modification of the inflammasome.

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