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
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pubmed:17433543Le document en format XML
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(drug effects)</term><term>RNA, Messenger (metabolism)</term><term>Superoxide Dismutase (genetics)</term><term>Superoxide Dismutase-1</term><term>Xanthones (pharmacology)</term><term>Xanthones (therapeutic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>1-Methyl-4-phenylpyridinium</term><term>Neurotoxins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Catalase</term><term>Superoxide Dismutase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Free Radical Scavengers</term><term>Glutathione</term><term>Glutathione Disulfide</term><term>Iron</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Neuroprotective 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xml:lang="en"><term>Iron Metabolism Disorders</term><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Mice</term><term>Superoxide Dismutase-1</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17433543</PMID><DateCreated><Year>2007</Year><Month>04</Month><Day>30</Day></DateCreated><DateCompleted><Year>2007</Year><Month>07</Month><Day>25</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0304-3940</ISSN><JournalIssue CitedMedium="Print"><Volume>418</Volume><Issue>2</Issue><PubDate><Year>2007</Year><Month>May</Month><Day>17</Day></PubDate></JournalIssue><Title>Neuroscience letters</Title><ISOAbbreviation>Neurosci. Lett.</ISOAbbreviation></Journal><ArticleTitle>Mangiferin protects against 1-methyl-4-phenylpyridinium toxicity mediated by oxidative stress in N2A cells.</ArticleTitle><Pagination><MedlinePgn>159-64</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Amazzal</LastName><ForeName>Laïla</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Laboratoire d'Ingénierie Moléculaire et Biochimie Pharmacologique, FR CNRS 2843, UFR SciFA, Université Paul Verlaine-Metz, Rue du Général Delestraint, 57070 Metz, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lapôtre</LastName><ForeName>Agnès</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Quignon</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Bagrel</LastName><ForeName>Denyse</ForeName><Initials>D</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal 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human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D044004">Xanthones</NameOfSubstance></Chemical><Chemical><RegistryNumber>1M84LD0UMD</RegistryNumber><NameOfSubstance UI="C013592">mangiferin</NameOfSubstance></Chemical><Chemical><RegistryNumber>E1UOL152H7</RegistryNumber><NameOfSubstance UI="D007501">Iron</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.6</RegistryNumber><NameOfSubstance UI="D002374">Catalase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="C000606291">Sod1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D000072105">Superoxide Dismutase-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical><Chemical><RegistryNumber>R865A5OY8J</RegistryNumber><NameOfSubstance UI="D015655">1-Methyl-4-phenylpyridinium</NameOfSubstance></Chemical><Chemical><RegistryNumber>ULW86O013H</RegistryNumber><NameOfSubstance UI="D019803">Glutathione Disulfide</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015655" MajorTopicYN="N">1-Methyl-4-phenylpyridinium</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002374" MajorTopicYN="N">Catalase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016166" MajorTopicYN="N">Free Radical Scavengers</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019803" MajorTopicYN="N">Glutathione Disulfide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007501" MajorTopicYN="N">Iron</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019189" MajorTopicYN="N">Iron Metabolism Disorders</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009410" MajorTopicYN="N">Nerve Degeneration</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018696" MajorTopicYN="N">Neuroprotective Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic 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PubStatus="accepted"><Year>2007</Year><Month>03</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>7</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>4</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17433543</ArticleId><ArticleId IdType="pii">S0304-3940(07)00319-9</ArticleId><ArticleId IdType="doi">10.1016/j.neulet.2007.03.025</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Grand Est</li><li>Lorraine (région)</li></region><settlement><li>Metz</li></settlement></list><tree><noCountry><name sortKey="Bagrel, Denyse" sort="Bagrel, Denyse" uniqKey="Bagrel D" 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