Protective Effect of Sulforaphane against Dopaminergic Cell Death
| العنوان: | Protective Effect of Sulforaphane against Dopaminergic Cell Death |
|---|---|
| المؤلفون: | Onyou Hwang, Eun Mee Kim, Yong Jin Lee, Ha Won Kim, Younghye Moon, So Yeon Lee, Ji Man Han |
| المصدر: | Journal of Pharmacology and Experimental Therapeutics. 321:249-256 |
| بيانات النشر: | American Society for Pharmacology & Experimental Therapeutics (ASPET), 2007. |
| سنة النشر: | 2007 |
| مصطلحات موضوعية: | Dopamine, Substantia nigra, DNA Fragmentation, Reductase, medicine.disease_cause, Chromosomes, chemistry.chemical_compound, Isothiocyanates, Dopaminergic Cell, medicine, Humans, Oxidopamine, Cells, Cultured, Pharmacology, chemistry.chemical_classification, Reactive oxygen species, Cell Death, L-Lactate Dehydrogenase, Reverse Transcriptase Polymerase Chain Reaction, Cell Membrane, Dopaminergic, Quinones, Tetrahydrobiopterin, Biopterin, Immunohistochemistry, Cell biology, Biochemistry, chemistry, Sulfoxides, Molecular Medicine, Reactive Oxygen Species, Thiocyanates, Oxidative stress, medicine.drug, Sulforaphane |
| الوصف: | Parkinson's disease (PD) is a progressive neurodegenerative disorder with a selective loss of dopaminergic neurons in the substantia nigra. Evidence suggests oxidation of dopamine (DA) to DA quinone and consequent oxidative stress as a major factor contributing to this vulnerability. We have previously observed that exposure to or induction of NAD(P)H:quinone reductase (QR1), the enzyme that catalyzes the reduction of quinone, effectively protects DA cells. Sulforaphane (SF) is a drug identified as a potent inducer of QR1 in various non-neuronal cells. In the present study, we show that SF protects against compounds known to induce DA quinone production (6-hydroxydopamine and tetrahydrobiopterin) in DAergic cell lines CATH.a and SK-N-BE(2)C as well as in mesencephalic DAergic neurons. SF leads to attenuation of the increase in protein-bound quinone in tetrahydrobiopterin-treated cells, but this does not occur in cells that have been depleted of DA, suggesting involvement of DA quinone. SF pretreatment prevents membrane damage, DNA fragmentation, and accumulation of reactive oxygen species. SF causes increases in mRNA levels and enzymatic activity of QR1 in a dose-dependent manner. Taken together, these results indicate that SF causes induction of QR1 gene expression, removal of intracellular DA quinone, and protection against toxicity in DAergic cells. Thus, this major isothiocyanate found in cruciferous vegetables may serve as a potential candidate for development of treatment and/or prevention of PD. |
| تدمد: | 1521-0103 0022-3565 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c521c6f6331da4df3358e1ba8d40f760Test https://doi.org/10.1124/jpet.106.110866Test |
| رقم الانضمام: | edsair.doi.dedup.....c521c6f6331da4df3358e1ba8d40f760 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15210103 00223565 |
|---|