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Protection against paraquat and A53T alpha-synuclein toxicity by cabergoline is partially mediated by dopamine receptors
- Source :
- Journal of the neurological sciences. 278(1-2)
- Publication Year :
- 2008
-
Abstract
- Both genetic and environmental factors are thought to be involved in the aetiology of Parkinson's disease (PD). Oxidative damage, mitochondrial and proteasomal dysfunction, and inflammatory change are considered to participate in PD pathogenesis. Dopamine agonists are used in the symptomatic treatment of PD but attention has recently also been focussed on their potential for use in slowing disease progression. We have studied the protective actions of the D2 dopamine agonist cabergoline in toxin (paraquat) and genetic (wild-type and mutant [A53T] alpha-synuclein) models of PD using SHSY-5Y cells. Cabergoline increased glutathione content, reduced free radical production and caspase-3 activation, increased mitochondrial membrane potential and ameliorated cell death in SHSY-5Y cells exposed to paraquat and this action was inhibited in part by D2 receptor blockade. Cabergoline also reduced the toxicity of wild-type and mutant alpha-synuclein expression following paraquat exposure by similar mechanisms. These results confirm the protective action of cabergoline in reducing cell death in two separate genetic and environmental model systems of PD.
- Subjects :
- Agonist
Paraquat
medicine.medical_specialty
Parkinson's disease
Cabergoline
medicine.drug_class
Blotting, Western
Apoptosis
Biology
Neuroprotection
Dopamine agonist
Cell Line
chemistry.chemical_compound
Parkinsonian Disorders
Internal medicine
Dopamine receptor D2
medicine
Humans
Ergolines
Lactate Dehydrogenases
Membrane Potential, Mitochondrial
Analysis of Variance
Caspase 3
Receptors, Dopamine D2
JNK Mitogen-Activated Protein Kinases
medicine.disease
Glutathione
Immunohistochemistry
Enzyme Activation
Endocrinology
Neurology
chemistry
Dopamine receptor
alpha-Synuclein
Neurology (clinical)
Reactive Oxygen Species
medicine.drug
Subjects
Details
- ISSN :
- 0022510X
- Volume :
- 278
- Issue :
- 1-2
- Database :
- OpenAIRE
- Journal :
- Journal of the neurological sciences
- Accession number :
- edsair.doi.dedup.....de87077026a073f66bc1181210a672e8