Bee venom and its component apamin as neuroprotective agents in a Parkinson disease mouse model.
Identifieur interne : 000744 ( PubMed/Corpus ); précédent : 000743; suivant : 000745Bee venom and its component apamin as neuroprotective agents in a Parkinson disease mouse model.
Auteurs : Daniel Alvarez-Fischer ; Carmen Noelker ; Franca Vulinovi ; Anne Grünewald ; Caroline Chevarin ; Christine Klein ; Wolfgang H. Oertel ; Etienne C. Hirsch ; Patrick P. Michel ; Andreas HartmannSource :
- PloS one [ 1932-6203 ] ; 2013.
English descriptors
- KwdEn :
- Acupuncture Points, Animals, Apamin (pharmacology), Bee Venoms (pharmacology), Behavior, Animal (drug effects), Corpus Striatum (drug effects), Corpus Striatum (metabolism), Disease Models, Animal, Dopaminergic Neurons (drug effects), Exploratory Behavior (drug effects), MPTP Poisoning (prevention & control), Male, Mice, Mice, Inbred C57BL, Neuroprotective Agents (pharmacology), Parkinson Disease (prevention & control), Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , metabolism : Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Apamin, Bee Venoms, Neuroprotective Agents.
- drug effects : Behavior, Animal, Corpus Striatum, Dopaminergic Neurons, Exploratory Behavior.
- metabolism : Corpus Striatum.
- prevention & control : MPTP Poisoning, Parkinson Disease.
- Acupuncture Points, Animals, Disease Models, Animal, Male, Mice, Mice, Inbred C57BL.
Abstract
Bee venom has recently been suggested to possess beneficial effects in the treatment of Parkinson disease (PD). For instance, it has been observed that bilateral acupoint stimulation of lower hind limbs with bee venom was protective in the acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. In particular, a specific component of bee venom, apamin, has previously been shown to have protective effects on dopaminergic neurons in vitro. However, no information regarding a potential protective action of apamin in animal models of PD is available to date. The specific goals of the present study were to (i) establish that the protective effect of bee venom for dopaminergic neurons is not restricted to acupoint stimulation, but can also be observed using a more conventional mode of administration and to (ii) demonstrate that apamin can mimic the protective effects of a bee venom treatment on dopaminergic neurons. Using the chronic mouse model of MPTP/probenecid, we show that bee venom provides sustained protection in an animal model that mimics the chronic degenerative process of PD. Apamin, however, reproduced these protective effects only partially, suggesting that other components of bee venom enhance the protective action of the peptide.
DOI: 10.1371/journal.pone.0061700
PubMed: 23637888
Links to Exploration step
pubmed:23637888Le document en format XML
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Oertel</name></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name></author><author><name sortKey="Michel, Patrick P" sort="Michel, Patrick P" uniqKey="Michel P" first="Patrick P" last="Michel">Patrick P. Michel</name></author><author><name sortKey="Hartmann, Andreas" sort="Hartmann, Andreas" uniqKey="Hartmann A" first="Andreas" last="Hartmann">Andreas Hartmann</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:23637888</idno><idno type="pmid">23637888</idno><idno type="doi">10.1371/journal.pone.0061700</idno><idno type="wicri:Area/PubMed/Corpus">000744</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000744</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Bee venom and its component apamin as neuroprotective agents in a Parkinson disease mouse model.</title><author><name sortKey="Alvarez Fischer, Daniel" sort="Alvarez Fischer, Daniel" uniqKey="Alvarez Fischer D" first="Daniel" last="Alvarez-Fischer">Daniel Alvarez-Fischer</name><affiliation><nlm:affiliation>Université Pierre et Marie Curie-Paris 6, UMR_S 975 - UMR 7725, Centre de Recherche en Neurosciences, ICM, Therapeutique Experimentale de la Neurodegenerescence, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Noelker, Carmen" sort="Noelker, Carmen" uniqKey="Noelker C" first="Carmen" last="Noelker">Carmen Noelker</name></author><author><name sortKey="Vulinovi, Franca" sort="Vulinovi, Franca" uniqKey="Vulinovi F" first="Franca" last="Vulinovi">Franca Vulinovi</name></author><author><name sortKey="Grunewald, Anne" sort="Grunewald, Anne" uniqKey="Grunewald A" first="Anne" last="Grünewald">Anne Grünewald</name></author><author><name sortKey="Chevarin, Caroline" sort="Chevarin, Caroline" uniqKey="Chevarin C" first="Caroline" last="Chevarin">Caroline Chevarin</name></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name></author><author><name sortKey="Oertel, Wolfgang H" sort="Oertel, Wolfgang H" uniqKey="Oertel W" first="Wolfgang H" last="Oertel">Wolfgang H. Oertel</name></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name></author><author><name sortKey="Michel, Patrick P" sort="Michel, Patrick P" uniqKey="Michel P" first="Patrick P" last="Michel">Patrick P. Michel</name></author><author><name sortKey="Hartmann, Andreas" sort="Hartmann, Andreas" uniqKey="Hartmann A" first="Andreas" last="Hartmann">Andreas Hartmann</name></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acupuncture Points</term><term>Animals</term><term>Apamin (pharmacology)</term><term>Bee Venoms (pharmacology)</term><term>Behavior, Animal (drug effects)</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (metabolism)</term><term>Disease Models, Animal</term><term>Dopaminergic Neurons (drug effects)</term><term>Exploratory Behavior (drug effects)</term><term>MPTP Poisoning (prevention & control)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Neuroprotective Agents (pharmacology)</term><term>Parkinson Disease (prevention & control)</term><term>Tumor Necrosis Factor-alpha (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Apamin</term><term>Bee Venoms</term><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Behavior, Animal</term><term>Corpus Striatum</term><term>Dopaminergic Neurons</term><term>Exploratory Behavior</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>MPTP Poisoning</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acupuncture Points</term><term>Animals</term><term>Disease Models, Animal</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Bee venom has recently been suggested to possess beneficial effects in the treatment of Parkinson disease (PD). For instance, it has been observed that bilateral acupoint stimulation of lower hind limbs with bee venom was protective in the acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. In particular, a specific component of bee venom, apamin, has previously been shown to have protective effects on dopaminergic neurons in vitro. However, no information regarding a potential protective action of apamin in animal models of PD is available to date. The specific goals of the present study were to (i) establish that the protective effect of bee venom for dopaminergic neurons is not restricted to acupoint stimulation, but can also be observed using a more conventional mode of administration and to (ii) demonstrate that apamin can mimic the protective effects of a bee venom treatment on dopaminergic neurons. Using the chronic mouse model of MPTP/probenecid, we show that bee venom provides sustained protection in an animal model that mimics the chronic degenerative process of PD. Apamin, however, reproduced these protective effects only partially, suggesting that other components of bee venom enhance the protective action of the peptide.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23637888</PMID><DateCreated><Year>2013</Year><Month>05</Month><Day>02</Day></DateCreated><DateCompleted><Year>2013</Year><Month>12</Month><Day>26</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>15</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>4</Issue><PubDate><Year>2013</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Bee venom and its component apamin as neuroprotective agents in a Parkinson disease mouse model.</ArticleTitle><Pagination><MedlinePgn>e61700</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0061700</ELocationID><Abstract><AbstractText>Bee venom has recently been suggested to possess beneficial effects in the treatment of Parkinson disease (PD). For instance, it has been observed that bilateral acupoint stimulation of lower hind limbs with bee venom was protective in the acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. In particular, a specific component of bee venom, apamin, has previously been shown to have protective effects on dopaminergic neurons in vitro. However, no information regarding a potential protective action of apamin in animal models of PD is available to date. The specific goals of the present study were to (i) establish that the protective effect of bee venom for dopaminergic neurons is not restricted to acupoint stimulation, but can also be observed using a more conventional mode of administration and to (ii) demonstrate that apamin can mimic the protective effects of a bee venom treatment on dopaminergic neurons. Using the chronic mouse model of MPTP/probenecid, we show that bee venom provides sustained protection in an animal model that mimics the chronic degenerative process of PD. Apamin, however, reproduced these protective effects only partially, suggesting that other components of bee venom enhance the protective action of the peptide.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Alvarez-Fischer</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Université Pierre et Marie Curie-Paris 6, UMR_S 975 - UMR 7725, Centre de Recherche en Neurosciences, ICM, Therapeutique Experimentale de la Neurodegenerescence, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Noelker</LastName><ForeName>Carmen</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Vulinović</LastName><ForeName>Franca</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Grünewald</LastName><ForeName>Anne</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Chevarin</LastName><ForeName>Caroline</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Klein</LastName><ForeName>Christine</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Oertel</LastName><ForeName>Wolfgang H</ForeName><Initials>WH</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>Etienne C</ForeName><Initials>EC</Initials></Author><Author ValidYN="Y"><LastName>Michel</LastName><ForeName>Patrick P</ForeName><Initials>PP</Initials></Author><Author ValidYN="Y"><LastName>Hartmann</LastName><ForeName>Andreas</ForeName><Initials>A</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>04</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001514">Bee Venoms</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>24345-16-2</RegistryNumber><NameOfSubstance UI="D001030">Apamin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2000 Nov 15;20(22):8493-503</RefSource><PMID 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