EGCG protects against 6‐OHDA induced neurotoxicity in a cell culture model
| العنوان: | EGCG protects against 6‐OHDA induced neurotoxicity in a cell culture model |
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| المؤلفون: | Manju B. Reddy, Anumantha G. Kanthasamy, Dan Chen |
| المصدر: | The FASEB Journal. 26 |
| بيانات النشر: | Wiley, 2012. |
| سنة النشر: | 2012 |
| مصطلحات موضوعية: | Neurite, biology, Chemistry, Dopaminergic, Cell, Neurotoxicity, DMT1, Pharmacology, medicine.disease, Biochemistry, medicine.anatomical_structure, nervous system, Hepcidin, Dopamine, Genetics, medicine, biology.protein, Molecular Biology, Intracellular, Biotechnology, medicine.drug |
| الوصف: | Background. Parkinson's disease (PD) is a progressive neurodegenerative disease that causes severe brain dopamine depletion. Disruption of iron metabolism may be involved in the PD progression. Objective. To test the protective effect of (-)-epigallocatechin-3-gallate (EGCG) against 6-hydroxydopamine- (6-OHDA-) induced neurotoxicity by regulating iron metabolism in N27 cells. Methods. Protection by EGCG in N27 cells was assessed by SYTOX green assay, MTT, and caspase-3 activity. Iron regulatory gene and protein expression were measured by RT-PCR and Western blotting. Intracellular iron uptake was measured using (55)Fe. The EGCG protection was further tested in primary mesencephalic dopaminergic neurons by immunocytochemistry. Results. EGCG protected against 6-OHDA-induced cell toxicity. 6-OHDA treatment significantly (p < 0.05) increased divalent metal transporter-1 (DMT1) and hepcidin and decreased ferroportin 1 (Fpn1) level, whereas pretreatment with EGCG counteracted the effects. The increased (55)Fe (by 96%, p < 0.01) cell uptake confirmed the iron burden by 6-OHDA and was reduced by EGCG by 27% (p < 0.05), supporting the DMT1 results. Pretreatment with EGCG and 6-OHDA significantly increased (p < 0.0001) TH(+) cell count (~3-fold) and neurite length (~12-fold) compared to 6-OHDA alone in primary mesencephalic neurons. Conclusions. Pretreatment with EGCG protected against 6-OHDA-induced neurotoxicity by regulating genes and proteins involved in brain iron homeostasis, especially modulating hepcidin levels. |
| تدمد: | 1530-6860 0892-6638 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_________::ac2f3dc6c984d0cf9520c23cbff9ca80Test https://doi.org/10.1096/fasebj.26.1_supplement.255.5Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi...........ac2f3dc6c984d0cf9520c23cbff9ca80 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15306860 08926638 |
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