Phenolic glycosides as inhibitors of inducible nitric oxide synthase from Populus davidiana in LPS-activated RAW 264.7 murine macrophages.
Identifieur interne : 002966 ( Main/Exploration ); précédent : 002965; suivant : 002967Phenolic glycosides as inhibitors of inducible nitric oxide synthase from Populus davidiana in LPS-activated RAW 264.7 murine macrophages.
Auteurs : Hwa Jin Lee [Corée du Sud] ; Ji Sun Kim ; Young-Kyoon Kim ; Jae-Ha RyuSource :
- Die Pharmazie [ 0031-7144 ] ; 2012.
Descripteurs français
- KwdFr :
- Activation des macrophages (effets des médicaments et des substances chimiques), Animaux (MeSH), Antienzymes (isolement et purification), Antienzymes (pharmacologie), Cellules cultivées (MeSH), Glucosides (isolement et purification), Glucosides (pharmacologie), Hétérosides (pharmacologie), Indicateurs et réactifs (MeSH), Lipopolysaccharides (pharmacologie), Macrophages (effets des médicaments et des substances chimiques), Macrophages (enzymologie), Monoxyde d'azote (biosynthèse), Nitric oxide synthase type II (antagonistes et inhibiteurs), Phénols (pharmacologie), Populus (composition chimique), Relation dose-effet des médicaments (MeSH), Solvants (MeSH), Souris (MeSH), Technique de Western (MeSH).
- MESH :
- antagonistes et inhibiteurs : Nitric oxide synthase type II.
- biosynthèse : Monoxyde d'azote.
- composition chimique : Populus.
- effets des médicaments et des substances chimiques : Activation des macrophages, Macrophages.
- enzymologie : Macrophages.
- isolement et purification : Antienzymes, Glucosides.
- pharmacologie : Antienzymes, Glucosides, Hétérosides, Lipopolysaccharides, Phénols.
- Animaux, Cellules cultivées, Indicateurs et réactifs, Relation dose-effet des médicaments, Solvants, Souris, Technique de Western.
English descriptors
- KwdEn :
- Animals (MeSH), Blotting, Western (MeSH), Cells, Cultured (MeSH), Dose-Response Relationship, Drug (MeSH), Enzyme Inhibitors (isolation & purification), Enzyme Inhibitors (pharmacology), Glucosides (isolation & purification), Glucosides (pharmacology), Glycosides (pharmacology), Indicators and Reagents (MeSH), Lipopolysaccharides (pharmacology), Macrophage Activation (drug effects), Macrophages (drug effects), Macrophages (enzymology), Mice (MeSH), Nitric Oxide (biosynthesis), Nitric Oxide Synthase Type II (antagonists & inhibitors), Phenols (pharmacology), Populus (chemistry), Solvents (MeSH).
- MESH :
- chemical , antagonists & inhibitors : Nitric Oxide Synthase Type II.
- chemical , biosynthesis : Nitric Oxide.
- chemical , isolation & purification : Enzyme Inhibitors, Glucosides.
- chemical , pharmacology : Enzyme Inhibitors, Glucosides, Glycosides, Lipopolysaccharides, Phenols.
- chemistry : Populus.
- drug effects : Macrophage Activation, Macrophages.
- enzymology : Macrophages.
- Animals, Blotting, Western, Cells, Cultured, Dose-Response Relationship, Drug, Indicators and Reagents, Mice, Solvents.
Abstract
Nitric oxide (NO) produced in large amounts by inducible nitric oxide synthase (i-NOS) is known to be responsible for the vasodilation and hypotension observed in septic shock and inflammation. Inhibitors of i-NOS, thus, may be useful candidates for the treatment of inflammatory diseases that accompany the overproduction of NO. Two phenolic glycosides, salicortin (1) and salicortin-6'-benzoate (2), were purified as active principles from the extracts of Populus davidiana by activity-guided purification procedures. They showed dose dependent inhibition of NO production in lipopolysaccharide (LPS)-activated RAW 264.7 cells. The IC50 values of salicortin (1) and salicortin-6'-benzoate (2) was 15 microM and over 50 microM, respectively. In immunoblot analysis, salicortin inhibited the expression of i-NOS. These new inhibitors of overproduction of NO may have potentials for the treatment of inflammation.
PubMed: 23136723
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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scheme="MESH" xml:lang="en"><term>Animals</term><term>Blotting, Western</term><term>Cells, Cultured</term><term>Dose-Response Relationship, Drug</term><term>Indicators and Reagents</term><term>Mice</term><term>Solvents</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Indicateurs et réactifs</term><term>Relation dose-effet des médicaments</term><term>Solvants</term><term>Souris</term><term>Technique de Western</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Nitric oxide (NO) produced in large amounts by inducible nitric oxide synthase (i-NOS) is known to be responsible for the vasodilation and hypotension observed in septic shock and inflammation. Inhibitors of i-NOS, thus, may be useful candidates for the treatment of inflammatory diseases that accompany the overproduction of NO. Two phenolic glycosides, salicortin (1) and salicortin-6'-benzoate (2), were purified as active principles from the extracts of Populus davidiana by activity-guided purification procedures. They showed dose dependent inhibition of NO production in lipopolysaccharide (LPS)-activated RAW 264.7 cells. The IC50 values of salicortin (1) and salicortin-6'-benzoate (2) was 15 microM and over 50 microM, respectively. In immunoblot analysis, salicortin inhibited the expression of i-NOS. 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Inhibitors of i-NOS, thus, may be useful candidates for the treatment of inflammatory diseases that accompany the overproduction of NO. Two phenolic glycosides, salicortin (1) and salicortin-6'-benzoate (2), were purified as active principles from the extracts of Populus davidiana by activity-guided purification procedures. They showed dose dependent inhibition of NO production in lipopolysaccharide (LPS)-activated RAW 264.7 cells. The IC50 values of salicortin (1) and salicortin-6'-benzoate (2) was 15 microM and over 50 microM, respectively. In immunoblot analysis, salicortin inhibited the expression of i-NOS. 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Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Pharmazie</MedlineTA><NlmUniqueID>9800766</NlmUniqueID><ISSNLinking>0031-7144</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004791">Enzyme Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005960">Glucosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006027">Glycosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007202">Indicators and Reagents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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IdType="pubmed">23136723</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Corée du Sud</li></country><region><li>Région capitale de Séoul</li></region><settlement><li>Séoul</li></settlement></list><tree><noCountry><name sortKey="Kim, Ji Sun" sort="Kim, Ji Sun" uniqKey="Kim J" first="Ji Sun" last="Kim">Ji Sun Kim</name><name sortKey="Kim, Young Kyoon" sort="Kim, Young Kyoon" uniqKey="Kim Y" first="Young-Kyoon" last="Kim">Young-Kyoon Kim</name><name sortKey="Ryu, Jae Ha" sort="Ryu, Jae Ha" uniqKey="Ryu J" first="Jae-Ha" last="Ryu">Jae-Ha Ryu</name></noCountry><country name="Corée du Sud"><region name="Région capitale de Séoul"><name sortKey="Lee, Hwa Jin" sort="Lee, Hwa Jin" uniqKey="Lee H" first="Hwa Jin" last="Lee">Hwa Jin Lee</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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