Salicortin inhibits osteoclast differentiation and bone resorption by down-regulating JNK and NF-κB/NFATc1 signaling pathways.
Identifieur interne : 001683 ( Main/Exploration ); précédent : 001682; suivant : 001684Salicortin inhibits osteoclast differentiation and bone resorption by down-regulating JNK and NF-κB/NFATc1 signaling pathways.
Auteurs : Shaobo Nie [République populaire de Chine] ; Jiawei Xu [République populaire de Chine] ; Chenghua Zhang [République populaire de Chine] ; Chen Xu [République populaire de Chine] ; Ming Liu [République populaire de Chine] ; Degang Yu [République populaire de Chine]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cellules cultivées (MeSH), Différenciation cellulaire (effets des médicaments et des substances chimiques), Facteur de transcription NF-kappa B (métabolisme), Facteurs de transcription NFATC (métabolisme), Glucosides (administration et posologie), Ostéoclastes (anatomopathologie), Ostéoclastes (effets des médicaments et des substances chimiques), Ostéoclastes (métabolisme), Relation dose-effet des médicaments (MeSH), Régulation négative (effets des médicaments et des substances chimiques), Résorption osseuse (anatomopathologie), Résorption osseuse (métabolisme), Résorption osseuse (prévention et contrôle), Souris (MeSH), Souris de lignée C57BL (MeSH), Système de signalisation des MAP kinases (effets des médicaments et des substances chimiques), Tibia (MeSH).
- MESH :
- administration et posologie : Glucosides.
- anatomopathologie : Ostéoclastes, Résorption osseuse.
- effets des médicaments et des substances chimiques : Différenciation cellulaire, Ostéoclastes, Régulation négative, Système de signalisation des MAP kinases.
- métabolisme : Facteur de transcription NF-kappa B, Facteurs de transcription NFATC, Ostéoclastes, Résorption osseuse.
- prévention et contrôle : Résorption osseuse.
- Animaux, Cellules cultivées, Relation dose-effet des médicaments, Souris, Souris de lignée C57BL, Tibia.
English descriptors
- KwdEn :
- Animals (MeSH), Bone Resorption (metabolism), Bone Resorption (pathology), Bone Resorption (prevention & control), Cell Differentiation (drug effects), Cells, Cultured (MeSH), Dose-Response Relationship, Drug (MeSH), Down-Regulation (drug effects), Glucosides (administration & dosage), MAP Kinase Signaling System (drug effects), Mice (MeSH), Mice, Inbred C57BL (MeSH), NF-kappa B (metabolism), NFATC Transcription Factors (metabolism), Osteoclasts (drug effects), Osteoclasts (metabolism), Osteoclasts (pathology), Tibia (MeSH).
- MESH :
- chemical , administration & dosage : Glucosides.
- drug effects : Cell Differentiation, Down-Regulation, MAP Kinase Signaling System, Osteoclasts.
- metabolism : Bone Resorption, NF-kappa B, NFATC Transcription Factors, Osteoclasts.
- pathology : Bone Resorption, Osteoclasts.
- prevention & control : Bone Resorption.
- Animals, Cells, Cultured, Dose-Response Relationship, Drug, Mice, Mice, Inbred C57BL, Tibia.
Abstract
Receptor activator of nuclear factor (NF)-κB ligand (RANKL)-activated signaling is essential for osteoclast differentiation, activation, and survival. Salicortin is a phenolic glycoside that has been isolated from many plants such as Populus and Salix species, and has been shown to have anti-amnesic and anti-adipogenic effects. In this study, we investigated the effect of salicortin on RANKL-induced osteoclasts formation, bone resorption, and activation of osteoclast-related signaling pathways. Salicortin suppressed RANKL-induced osteoclastogenesis in bone marrow macrophage cultures in a dose-dependent manner, and inhibited osteoclastic bone resorption activity without any cytotoxicity. Salicortin inhibited RANKL-induced c-Jun N-terminal kinase and NF-κB activation, concomitant with retarded IκBα phosphorylation and inhibition of p65 nuclear translocation, leading to impaired transcription of nuclear factor of activated T cells c1 (NFATc1) and expression of osteoclastic-specific genes. Taken together, our findings demonstrate that salicortin inhibits NF-κB and NFATc1 activation, leading to attenuation of osteoclastogenesis and bone resorption. Thus, salicortin may be of interest in developments of treatment for osteoclast related diseases.
DOI: 10.1016/j.bbrc.2015.12.115
PubMed: 26740180
Affiliations:
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Salicortin is a phenolic glycoside that has been isolated from many plants such as Populus and Salix species, and has been shown to have anti-amnesic and anti-adipogenic effects. In this study, we investigated the effect of salicortin on RANKL-induced osteoclasts formation, bone resorption, and activation of osteoclast-related signaling pathways. Salicortin suppressed RANKL-induced osteoclastogenesis in bone marrow macrophage cultures in a dose-dependent manner, and inhibited osteoclastic bone resorption activity without any cytotoxicity. Salicortin inhibited RANKL-induced c-Jun N-terminal kinase and NF-κB activation, concomitant with retarded IκBα phosphorylation and inhibition of p65 nuclear translocation, leading to impaired transcription of nuclear factor of activated T cells c1 (NFATc1) and expression of osteoclastic-specific genes. Taken together, our findings demonstrate that salicortin inhibits NF-κB and NFATc1 activation, leading to attenuation of osteoclastogenesis and bone resorption. Thus, salicortin may be of interest in developments of treatment for osteoclast related diseases. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26740180</PMID><DateCompleted><Year>2016</Year><Month>06</Month><Day>07</Day></DateCompleted><DateRevised><Year>2018</Year><Month>09</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>470</Volume><Issue>1</Issue><PubDate><Year>2016</Year><Month>Jan</Month><Day>29</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>Salicortin inhibits osteoclast differentiation and bone resorption by down-regulating JNK and NF-κB/NFATc1 signaling pathways.</ArticleTitle><Pagination><MedlinePgn>61-67</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(15)31120-7</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2015.12.115</ELocationID><Abstract><AbstractText>Receptor activator of nuclear factor (NF)-κB ligand (RANKL)-activated signaling is essential for osteoclast differentiation, activation, and survival. Salicortin is a phenolic glycoside that has been isolated from many plants such as Populus and Salix species, and has been shown to have anti-amnesic and anti-adipogenic effects. In this study, we investigated the effect of salicortin on RANKL-induced osteoclasts formation, bone resorption, and activation of osteoclast-related signaling pathways. Salicortin suppressed RANKL-induced osteoclastogenesis in bone marrow macrophage cultures in a dose-dependent manner, and inhibited osteoclastic bone resorption activity without any cytotoxicity. Salicortin inhibited RANKL-induced c-Jun N-terminal kinase and NF-κB activation, concomitant with retarded IκBα phosphorylation and inhibition of p65 nuclear translocation, leading to impaired transcription of nuclear factor of activated T cells c1 (NFATc1) and expression of osteoclastic-specific genes. Taken together, our findings demonstrate that salicortin inhibits NF-κB and NFATc1 activation, leading to attenuation of osteoclastogenesis and bone resorption. Thus, salicortin may be of interest in developments of treatment for osteoclast related diseases. </AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nie</LastName><ForeName>Shaobo</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Orthopaedics, PLA General Hospital, Beijing 100853, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Jiawei</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Orthopaedics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, PRChina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Chenghua</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Orthopaedics, Changle County Hospital of Traditional Chinese Medicine, Weifang 262400, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Chen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Orthopaedics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, PRChina.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Ming</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Orthopaedics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, PRChina. Electronic address: ming_li4717@sina.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Degang</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Orthopaedics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, PRChina. Electronic address: ydg163@126.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>12</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005960">Glucosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050778">NFATC Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494005">Nfatc1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>YI29948E0Q</RegistryNumber><NameOfSubstance UI="C113068">salicortin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001862" MajorTopicYN="N">Bone Resorption</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005960" MajorTopicYN="N">Glucosides</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020935" MajorTopicYN="N">MAP Kinase Signaling System</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050778" MajorTopicYN="N">NFATC Transcription Factors</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010010" MajorTopicYN="N">Osteoclasts</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013977" MajorTopicYN="N">Tibia</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">JNK</Keyword><Keyword MajorTopicYN="N">NF-κB/NFATc1</Keyword><Keyword MajorTopicYN="N">Osteoclastogenesis</Keyword><Keyword MajorTopicYN="N">Salicortin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>12</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>12</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>1</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>1</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>6</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26740180</ArticleId><ArticleId IdType="pii">S0006-291X(15)31120-7</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2015.12.115</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Nie, Shaobo" sort="Nie, Shaobo" uniqKey="Nie S" first="Shaobo" last="Nie">Shaobo Nie</name></noRegion><name sortKey="Liu, Ming" sort="Liu, Ming" uniqKey="Liu M" first="Ming" last="Liu">Ming Liu</name><name sortKey="Xu, Chen" sort="Xu, Chen" uniqKey="Xu C" first="Chen" last="Xu">Chen Xu</name><name sortKey="Xu, Jiawei" sort="Xu, Jiawei" uniqKey="Xu J" first="Jiawei" last="Xu">Jiawei Xu</name><name sortKey="Yu, Degang" sort="Yu, Degang" uniqKey="Yu D" first="Degang" last="Yu">Degang Yu</name><name sortKey="Zhang, Chenghua" sort="Zhang, Chenghua" uniqKey="Zhang C" first="Chenghua" last="Zhang">Chenghua Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Salicortin inhibits osteoclast differentiation and bone resorption by down-regulating JNK and NF-κB/NFATc1 signaling pathways.
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