We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Neuroprotective effect ofl-dopa on dopaminergic neurons is comparable to pramipexol in MPTP-treated animal model of Parkinson’s disease: a direct comparison study.
- Authors
Jin Young Shin; Hyun-Jung Park; Young Hwan Ahn; Phil Hyu Lee
- Abstract
Parkinson’s disease (PD) is a chronic neurodegenerative disease characterized by selective loss of dopaminergic neurons in the pars compacta of the substantia nigra. Levodopa (l-dopa) and dopamine agonists have been most commonly used for symptomatic treatment. However, there are discrepancies between clinical and experimental data with respect to the neuroprotective effects of these drugs on dopaminergic neurons. In this study, to determine whetherl-dopa is toxic or dopamine agonist is neuroprotective to dopaminergic neurons, we evaluated the neuroprotective properties ofl-dopa and the pramipexol (PPX), one of dopamine agonists, with a focus on the regulatory effects of the anti-oxidant properties and cell survival or apoptotic signal pathways in the same experimental design, using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated PD animals. The glutathione level in MPTP-treated mice was significantly increased by PPX administration but not by L-dopa treatment. The expression of phosphorylated extracellular signal regulated kinase in MPTP-treated mice was significantly increased only withl-dopa treatment. Treatment with eitherl-dopa or PPX in MPTP-treated mice led to significantly decreased expressions of JNK phosphorylation, Bax, and cytochrome c and to an increased level of Bcl-2 expression with a similar degree, compared with the levels in MPTP-only treated mice. Immunohistochemical analysis showed that bothl-dopa and PPX increased significantly survival of dopaminergic neurons in MPTP-treated mice. Our study demonstrated that bothl-dopa and PPX had comparable neuroprotective properties for dopaminergic neurons in MPTP-treated PD animal models, through modulation of cell survival and apoptotic pathways.
- Publication
Journal of Neurochemistry, 2009, Vol 111, Issue 4, p1042
- ISSN
0022-3042
- Publication type
Academic Journal
- DOI
10.1111/j.1471-4159.2009.06381.x