EN
Parkinson’s disease (PD) is a progressive degenerative disorder, which etiology and pathogenesis remains unknown. Post mortem analysis of PD brain and studies on neurotoxic animal models of PD have provided evidence to support the involvement of oxidative stress and neuroinflammatory processes in the pathogenesis of PD. The high level of nitric oxide (NO) is produced by iNOS during the neuroinflammatory process caused by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) treatment. Under pathological condition NO can easily react with superoxide to form peroxynitrite (ONOOˉ), which is a strong oxidant. In the present study was examined the influence of the increased concentration of IL-10 (an anti-inflammatory cytokine) on the NOS expression in mouse model of PD induced by MPTP. One year-old male C57Bl mice were used in this study. An adeno-associated viral vector expressing the gene for human interleukin-10 (hIL-10) was used to transduce striatal cells 4 weeks prior to MPTP intoxication. Mice were sacrificed at the different time intervals: 1, 7 and 21 days after MPTP injection. Immunohistochemical and western blot analyses provide evidence for the protective properties of AAV2-hIL-10 in the MPTP-induced model of PD. There were reduction in the dopaminergic neuron quantity in SNpc and tyrosine hydroxylase protein in the striatum after MPTP injections, whereas in the group additionally treated with AAV2-hIL10 neuroprotection was observed. Treatment with AAV2-hIL-10 suppressed the MPTP-induced increase in iNOS and 3-nitrotyrosine (3-NT) expression in the midbrain.