ParkinsonFranceV1, Hal, Corpus, bibRecord, 000A70

Supramolecular Inhibition of Neurodegeneration by a Synthetic Receptor

Identifieur interne : 000A70 ( Hal/Corpus ); précédent : 000A69; suivant : 000A71

Supramolecular Inhibition of Neurodegeneration by a Synthetic Receptor

Auteurs : Shengke Li ; Huanxian Chen ; Xue Yang ; David Bardelang ; Ian W. Wyman ; Jianbo Wan ; Simon M. Y. Lee ; Ruibing Wang

Source :

ACS Medicinal Chemistry Letters [ 1948-5875 ] ; 2015-12-10.

RBID : Hal:hal-01414666

English descriptors

mix :
- Neurodegeneration, cucurbituril, inhibition, neurotoxin, supramolecular complexation.

Abstract

Cucurbit[7]uril (CB[7]) was found in vitro to sequester the neurotoxins MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and MPP+ (N-methyl-4-phenylpyridine). The CB[7]/neurotoxin host–guest complexes were studied in detail with 1H NMR, electrospray ionization mass spectrometry, UV–visible spectroscopic titration, and molecular modeling by density functional theory. The results supported the macrocyclic encapsulation of MPTP and MPP+, respectively, by CB[7] in aqueous solutions with relatively strong affinities and 1:1 host–guest binding stoichiometries in both cases. More importantly, the progression of MPTP/MPP+ induced neurodegeneration (often referred to as a Parkinson’s disease model) was observed to be strongly inhibited in vivo by the synthetic CB[7] receptor, as shown in zebrafish models. These results show that a supramolecular approach could lead to a new preventive and/or therapeutic strategy for counteracting the deleterious effects of some neurotoxins leading to neurodegeneration.

Url:

https://hal.archives-ouvertes.fr/hal-01414666

DOI: 10.1021/acsmedchemlett.5b00372

Links to Exploration step

Hal:hal-01414666

Le document en format XML

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<profileDesc><textClass><keywords scheme="mix" xml:lang="en"><term> Neurodegeneration</term>
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<front><div type="abstract" xml:lang="en">Cucurbit[7]uril (CB[7]) was found in vitro to sequester the neurotoxins MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and MPP+ (N-methyl-4-phenylpyridine). The CB[7]/neurotoxin host–guest complexes were studied in detail with 1H NMR, electrospray ionization mass spectrometry, UV–visible spectroscopic titration, and molecular modeling by density functional theory. The results supported the macrocyclic encapsulation of MPTP and MPP+, respectively, by CB[7] in aqueous solutions with relatively strong affinities and 1:1 host–guest binding stoichiometries in both cases. More importantly, the progression of MPTP/MPP+ induced neurodegeneration (often referred to as a Parkinson’s disease model) was observed to be strongly inhibited in vivo by the synthetic CB[7] receptor, as shown in zebrafish models. These results show that a supramolecular approach could lead to a new preventive and/or therapeutic strategy for counteracting the deleterious effects of some neurotoxins leading to neurodegeneration.</div>
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            <idno type="halRefHtml">ACS Medicinal Chemistry Letters, American Chemical Society, 2015, 6 (12), pp.1174 - 1178. <10.1021/acsmedchemlett.5b00372></idno>
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          <seriesStmt>            <idno type="stamp" n="CNRS">CNRS - Centre national de la recherche scientifique</idno>
            <idno type="stamp" n="UNIV-AMU">Aix Marseille Université</idno>
            <idno type="stamp" n="INC-CNRS">Institut de Chimie du CNRS</idno>
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          <sourceDesc>            <biblStruct>              <analytic>                <title xml:lang="en">Supramolecular Inhibition of Neurodegeneration by a Synthetic Receptor</title>
                <author role="aut">                  <persName>                    <forename type="first">Shengke</forename>
                    <surname>Li</surname>
                  </persName>
                  <idno type="halauthorid">1409346</idno>
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                </author>
                <author role="aut">                  <persName>                    <forename type="first">Huanxian</forename>
                    <surname>Chen</surname>
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                  <affiliation ref="#struct-475782"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Xue</forename>
                    <surname>Yang</surname>
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                  <affiliation ref="#struct-475782"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">David</forename>
                    <surname>Bardelang</surname>
                  </persName>
                  <idno type="halauthorid">1409350</idno>
                  <affiliation ref="#struct-258556"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Ian W.</forename>
                    <surname>Wyman</surname>
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                <author role="aut">                  <persName>                    <forename type="first">Jianbo</forename>
                    <surname>Wan</surname>
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                </author>
                <author role="aut">                  <persName>                    <forename type="first">Simon M. Y.</forename>
                    <surname>Lee</surname>
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                  <idno type="halauthorid">1432834</idno>
                  <affiliation ref="#struct-475782"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Ruibing</forename>
                    <surname>Wang</surname>
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                </author>
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              <monogr>                <idno type="halJournalId" status="VALID">102193</idno>
                <idno type="issn">1948-5875</idno>
                <title level="j">ACS Medicinal Chemistry Letters</title>
                <imprint>                  <publisher>American Chemical Society</publisher>
                  <biblScope unit="volume">6</biblScope>
                  <biblScope unit="issue">12</biblScope>
                  <biblScope unit="pp">1174 - 1178</biblScope>
                  <date type="datePub">2015-12-10</date>
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              <idno type="doi">10.1021/acsmedchemlett.5b00372</idno>
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            <textClass>              <keywords scheme="author">                <term xml:lang="en"> cucurbituril</term>
                <term xml:lang="en"> inhibition</term>
                <term xml:lang="en"> Neurodegeneration</term>
                <term xml:lang="en"> neurotoxin</term>
                <term xml:lang="en"> supramolecular complexation</term>
              </keywords>
              <classCode scheme="halDomain" n="chim">Chemical Sciences</classCode>
              <classCode scheme="halTypology" n="ART">Journal articles</classCode>
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            <abstract xml:lang="en">Cucurbit[7]uril (CB[7]) was found in vitro to sequester the neurotoxins MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and MPP+ (N-methyl-4-phenylpyridine). The CB[7]/neurotoxin host–guest complexes were studied in detail with 1H NMR, electrospray ionization mass spectrometry, UV–visible spectroscopic titration, and molecular modeling by density functional theory. The results supported the macrocyclic encapsulation of MPTP and MPP+, respectively, by CB[7] in aqueous solutions with relatively strong affinities and 1:1 host–guest binding stoichiometries in both cases. More importantly, the progression of MPTP/MPP+ induced neurodegeneration (often referred to as a Parkinson’s disease model) was observed to be strongly inhibited in vivo by the synthetic CB[7] receptor, as shown in zebrafish models. These results show that a supramolecular approach could lead to a new preventive and/or therapeutic strategy for counteracting the deleterious effects of some neurotoxins leading to neurodegeneration.</abstract>
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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Supramolecular Inhibition of Neurodegeneration by a Synthetic Receptor

Supramolecular Inhibition of Neurodegeneration by a Synthetic Receptor

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