Mangiferin protects against 1-methyl-4-phenylpyridinium toxicity mediated by oxidative stress in N2A cells.
Identifieur interne : 000719 ( Ncbi/Merge ); précédent : 000718; suivant : 000720Mangiferin protects against 1-methyl-4-phenylpyridinium toxicity mediated by oxidative stress in N2A cells.
Auteurs : Laïla Amazzal [France] ; Agnès Lapôtre ; Frédéric Quignon ; Denyse BagrelSource :
- Neuroscience letters [ 0304-3940 ] ; 2007.
English descriptors
- KwdEn :
- 1-Methyl-4-phenylpyridinium (antagonists & inhibitors), 1-Methyl-4-phenylpyridinium (toxicity), Animals, Catalase (genetics), Cell Line, Tumor, Free Radical Scavengers (metabolism), Glutathione (metabolism), Glutathione Disulfide (metabolism), Iron (metabolism), Iron Metabolism Disorders (drug therapy), Iron Metabolism Disorders (metabolism), Iron Metabolism Disorders (physiopathology), Mice, Nerve Degeneration (drug therapy), Nerve Degeneration (metabolism), Nerve Degeneration (physiopathology), Neurons (drug effects), Neurons (metabolism), Neuroprotective Agents (pharmacology), Neuroprotective Agents (therapeutic use), Neurotoxins (antagonists & inhibitors), Neurotoxins (toxicity), Oxidative Stress (drug effects), Oxidative Stress (physiology), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), RNA, Messenger (drug effects), RNA, Messenger (metabolism), Superoxide Dismutase (genetics), Superoxide Dismutase-1, Xanthones (pharmacology), Xanthones (therapeutic use).
- MESH :
- chemical , antagonists & inhibitors : 1-Methyl-4-phenylpyridinium, Neurotoxins.
- chemical , drug effects : RNA, Messenger.
- chemical , genetics : Catalase, Superoxide Dismutase.
- chemical , metabolism : Free Radical Scavengers, Glutathione, Glutathione Disulfide, Iron, RNA, Messenger.
- chemical , pharmacology : Neuroprotective Agents, Xanthones.
- chemical , therapeutic use : Neuroprotective Agents, Xanthones.
- chemical , toxicity : 1-Methyl-4-phenylpyridinium, Neurotoxins.
- drug effects : Neurons, Oxidative Stress.
- drug therapy : Iron Metabolism Disorders, Nerve Degeneration, Parkinson Disease.
- metabolism : Iron Metabolism Disorders, Nerve Degeneration, Neurons, Parkinson Disease.
- physiology : Oxidative Stress.
- physiopathology : Iron Metabolism Disorders, Nerve Degeneration, Parkinson Disease.
- Animals, Cell Line, Tumor, Mice, Superoxide Dismutase-1.
Abstract
1-Methyl-4-phenyl-pyridine ion (MPP+), the active metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces a Parkinsonian syndrome in humans and animals, a neurotoxic effect postulated to derive from oxidative stress. We report here the first investigation of MPP+-induced oxidative stress in the murine neuroblastoma cell line N2A. Significant cell death was observed following exposure to 0.25 mM MPP+. Markers of oxidative stress included decreased intracellular levels of GSH after 48 h of exposure (85% depletion) as well as an increase in GSSG. Expression of both superoxide dismutase 1 (sod1) and catalase (cat) mRNA was increased, as well the activity of catalase. These cellular effects were, at least partially, reversed by treatment with the natural polyphenol mangiferin. Administration of mangiferin protected N2A cells against MPP+-induced cytotoxicity, restored the GSH content (to 60% of control levels), and down-regulated both sod1 and cat mRNA expression. Together, these results suggest that the protective effect of mangiferin in N2A cells is mediated by the quenching of reactive oxygen intermediates. Therefore, mangiferin could be a useful compound in therapies for degenerative diseases, including Parkinson's disease, in which oxidative stress plays a crucial role.
DOI: 10.1016/j.neulet.2007.03.025
PubMed: 17433543
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000D83
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Links to Exploration step
pubmed:17433543Le document en format XML
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<front><div type="abstract" xml:lang="en">1-Methyl-4-phenyl-pyridine ion (MPP+), the active metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces a Parkinsonian syndrome in humans and animals, a neurotoxic effect postulated to derive from oxidative stress. We report here the first investigation of MPP+-induced oxidative stress in the murine neuroblastoma cell line N2A. Significant cell death was observed following exposure to 0.25 mM MPP+. Markers of oxidative stress included decreased intracellular levels of GSH after 48 h of exposure (85% depletion) as well as an increase in GSSG. Expression of both superoxide dismutase 1 (sod1) and catalase (cat) mRNA was increased, as well the activity of catalase. These cellular effects were, at least partially, reversed by treatment with the natural polyphenol mangiferin. Administration of mangiferin protected N2A cells against MPP+-induced cytotoxicity, restored the GSH content (to 60% of control levels), and down-regulated both sod1 and cat mRNA expression. Together, these results suggest that the protective effect of mangiferin in N2A cells is mediated by the quenching of reactive oxygen intermediates. Therefore, mangiferin could be a useful compound in therapies for degenerative diseases, including Parkinson's disease, in which oxidative stress plays a crucial role.</div>
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<name sortKey="Quignon, Frederic" sort="Quignon, Frederic" uniqKey="Quignon F" first="Frédéric" last="Quignon">Frédéric Quignon</name>
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<country name="France"><region name="Grand Est"><name sortKey="Amazzal, Laila" sort="Amazzal, Laila" uniqKey="Amazzal L" first="Laïla" last="Amazzal">Laïla Amazzal</name>
</region>
</country>
</tree>
</affiliations>
</record>
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