Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways
Over‐activated osteoclastogenesis, which is initiated by inflammation, has been implicated in osteoporosis. Corilagin, a natural compound extracted from various medicinal herbaceous plants, such as Cinnamomum cassia, has antioxidant and anti‐inflammatory activities. We found that Corilagin suppresse...
Gespeichert in:
| Veröffentlicht in: | Journal of cellular and molecular medicine 2020-09, Vol.24 (18), p.10444-10457 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 10457 |
|---|---|
| container_issue | 18 |
| container_start_page | 10444 |
| container_title | Journal of cellular and molecular medicine |
| container_volume | 24 |
| creator | Lu, Jinwei Ye, Chenyi Huang, Yanyong Huang, Donghui Tang, Lan Hou, Weiduo Kuang, Zhihui Chen, Yazhou Xiao, Shining Yishake, Mumingjiang He, Rongxin |
| description | Over‐activated osteoclastogenesis, which is initiated by inflammation, has been implicated in osteoporosis. Corilagin, a natural compound extracted from various medicinal herbaceous plants, such as Cinnamomum cassia, has antioxidant and anti‐inflammatory activities. We found that Corilagin suppressed osteoclast differentiation in a dose‐dependent manner, significantly decreased osteoclast‐related gene expression and impaired bone resorption by osteoclasts. Moreover, phosphorylation of members of the nuclear factor‐kappaB (NF‐κB) and PI3K/AKT signalling pathways was reduced by Corilagin. In a murine model of osteoporosis, Corilagin inhibited osteoclast functions in vivo and restored oestrogen deficiency‐induced bone loss. In conclusion, our findings suggested that Corilagin inhibited osteoclastogenesis by down‐regulating the NF‐κB and PI3K/AKT signalling pathways, thus showing its potential possibility for the treatment of osteoporosis. |
| doi_str_mv | 10.1111/jcmm.15657 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7521306</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2446628693</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4767-13bf4c43fe1cc4daa78cded4cda48a062cfc8240111c079a644267a538a4df333</originalsourceid><addsrcrecordid>eNp9kk9uEzEYxUcIREthwwGQJTYIKe34z9ieDVKIKJSkBaGythzbM3Hk2FN7plV2HIEb9B49BIfgJDhNqAqLemNL7-en73t6RfESlocwn6OlWq0OYUUr9qjYhxVHI1Jj8nj3hhzzveJZSsuyxBTi-mmxhxHlkEK0X1xPQrROttaDNHRdNCmZBL6Nz6az3z9-Wq8HZTQIqTdBOZn60Bpvkk1Aeg2sX9i57RMIJvVxIwFtGqus8Wp97_s8eANcSAlcWgn6hQFnx1n-dfP-1ubrCZ4ejafnINnWS-esb0En-8WVXKfnxZNGumRe7O6D4vvxh_PJp9Hsy8eTyXg2UoRRNoJ43hBFcGOgUkRLybjSRhOlJeGypEg1iiNS5rhUyWpJCUGUyQpzSXSDMT4o3m19u2G-MloZ30fpRBftSsa1CNKKfxVvF6INl4JVCOKSZoM3O4MYLoach1jZpIxz0pswJIEIInXNEOcZff0fugxDzJtnijFcEcLIwxQhlCJO683cb7eUijnfaJq7kWEpNu0Qm3aI23Zk-NX9Je_Qv3XIANwCV9aZ9QNW4vPk9HRr-gfDystY</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2446628693</pqid></control><display><type>article</type><title>Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways</title><source>MEDLINE</source><source>Wiley Online Library Open Access</source><source>DOAJ Directory of Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Lu, Jinwei ; Ye, Chenyi ; Huang, Yanyong ; Huang, Donghui ; Tang, Lan ; Hou, Weiduo ; Kuang, Zhihui ; Chen, Yazhou ; Xiao, Shining ; Yishake, Mumingjiang ; He, Rongxin</creator><creatorcontrib>Lu, Jinwei ; Ye, Chenyi ; Huang, Yanyong ; Huang, Donghui ; Tang, Lan ; Hou, Weiduo ; Kuang, Zhihui ; Chen, Yazhou ; Xiao, Shining ; Yishake, Mumingjiang ; He, Rongxin</creatorcontrib><description>Over‐activated osteoclastogenesis, which is initiated by inflammation, has been implicated in osteoporosis. Corilagin, a natural compound extracted from various medicinal herbaceous plants, such as Cinnamomum cassia, has antioxidant and anti‐inflammatory activities. We found that Corilagin suppressed osteoclast differentiation in a dose‐dependent manner, significantly decreased osteoclast‐related gene expression and impaired bone resorption by osteoclasts. Moreover, phosphorylation of members of the nuclear factor‐kappaB (NF‐κB) and PI3K/AKT signalling pathways was reduced by Corilagin. In a murine model of osteoporosis, Corilagin inhibited osteoclast functions in vivo and restored oestrogen deficiency‐induced bone loss. In conclusion, our findings suggested that Corilagin inhibited osteoclastogenesis by down‐regulating the NF‐κB and PI3K/AKT signalling pathways, thus showing its potential possibility for the treatment of osteoporosis.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.15657</identifier><identifier>PMID: 32681612</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; Actins - metabolism ; AKT protein ; Animal models ; Animals ; Antibodies ; Antioxidants ; Bone loss ; Bone Marrow Cells - drug effects ; Bone Marrow Cells - metabolism ; Bone resorption ; Bone Resorption - pathology ; Corilagin ; Down-Regulation - drug effects ; Estrogens ; Estrogens - deficiency ; Gene expression ; Glucosides - chemistry ; Glucosides - pharmacology ; Hydrolyzable Tannins - chemistry ; Hydrolyzable Tannins - pharmacology ; Inflammation ; Laboratory animals ; Medicinal plants ; Mice ; Mice, Inbred C57BL ; NF-kappa B - metabolism ; NF-κB protein ; NFATC Transcription Factors - metabolism ; NF‐κB ; Oophorectomy ; Original ; osteoclast ; Osteoclastogenesis ; Osteoclasts ; Osteoclasts - drug effects ; Osteoclasts - metabolism ; Osteoclasts - pathology ; Osteogenesis - drug effects ; Osteoporosis ; Osteoprotegerin - metabolism ; Ovariectomy ; Phosphatase ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; PI3K/AKT ; Proto-Oncogene Proteins c-akt - metabolism ; RANK Ligand - pharmacology ; RANKL ; RAW 264.7 Cells ; Reactive Oxygen Species - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal transduction ; Signal Transduction - drug effects ; TRANCE protein ; Tumor necrosis factor-TNF</subject><ispartof>Journal of cellular and molecular medicine, 2020-09, Vol.24 (18), p.10444-10457</ispartof><rights>2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd</rights><rights>2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4767-13bf4c43fe1cc4daa78cded4cda48a062cfc8240111c079a644267a538a4df333</citedby><cites>FETCH-LOGICAL-c4767-13bf4c43fe1cc4daa78cded4cda48a062cfc8240111c079a644267a538a4df333</cites><orcidid>0000-0002-5937-3878</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521306/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7521306/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11542,27903,27904,45553,45554,46030,46454,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32681612$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Jinwei</creatorcontrib><creatorcontrib>Ye, Chenyi</creatorcontrib><creatorcontrib>Huang, Yanyong</creatorcontrib><creatorcontrib>Huang, Donghui</creatorcontrib><creatorcontrib>Tang, Lan</creatorcontrib><creatorcontrib>Hou, Weiduo</creatorcontrib><creatorcontrib>Kuang, Zhihui</creatorcontrib><creatorcontrib>Chen, Yazhou</creatorcontrib><creatorcontrib>Xiao, Shining</creatorcontrib><creatorcontrib>Yishake, Mumingjiang</creatorcontrib><creatorcontrib>He, Rongxin</creatorcontrib><title>Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Over‐activated osteoclastogenesis, which is initiated by inflammation, has been implicated in osteoporosis. Corilagin, a natural compound extracted from various medicinal herbaceous plants, such as Cinnamomum cassia, has antioxidant and anti‐inflammatory activities. We found that Corilagin suppressed osteoclast differentiation in a dose‐dependent manner, significantly decreased osteoclast‐related gene expression and impaired bone resorption by osteoclasts. Moreover, phosphorylation of members of the nuclear factor‐kappaB (NF‐κB) and PI3K/AKT signalling pathways was reduced by Corilagin. In a murine model of osteoporosis, Corilagin inhibited osteoclast functions in vivo and restored oestrogen deficiency‐induced bone loss. In conclusion, our findings suggested that Corilagin inhibited osteoclastogenesis by down‐regulating the NF‐κB and PI3K/AKT signalling pathways, thus showing its potential possibility for the treatment of osteoporosis.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Actins - metabolism</subject><subject>AKT protein</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antioxidants</subject><subject>Bone loss</subject><subject>Bone Marrow Cells - drug effects</subject><subject>Bone Marrow Cells - metabolism</subject><subject>Bone resorption</subject><subject>Bone Resorption - pathology</subject><subject>Corilagin</subject><subject>Down-Regulation - drug effects</subject><subject>Estrogens</subject><subject>Estrogens - deficiency</subject><subject>Gene expression</subject><subject>Glucosides - chemistry</subject><subject>Glucosides - pharmacology</subject><subject>Hydrolyzable Tannins - chemistry</subject><subject>Hydrolyzable Tannins - pharmacology</subject><subject>Inflammation</subject><subject>Laboratory animals</subject><subject>Medicinal plants</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>NFATC Transcription Factors - metabolism</subject><subject>NF‐κB</subject><subject>Oophorectomy</subject><subject>Original</subject><subject>osteoclast</subject><subject>Osteoclastogenesis</subject><subject>Osteoclasts</subject><subject>Osteoclasts - drug effects</subject><subject>Osteoclasts - metabolism</subject><subject>Osteoclasts - pathology</subject><subject>Osteogenesis - drug effects</subject><subject>Osteoporosis</subject><subject>Osteoprotegerin - metabolism</subject><subject>Ovariectomy</subject><subject>Phosphatase</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>PI3K/AKT</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>RANK Ligand - pharmacology</subject><subject>RANKL</subject><subject>RAW 264.7 Cells</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>TRANCE protein</subject><subject>Tumor necrosis factor-TNF</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kk9uEzEYxUcIREthwwGQJTYIKe34z9ieDVKIKJSkBaGythzbM3Hk2FN7plV2HIEb9B49BIfgJDhNqAqLemNL7-en73t6RfESlocwn6OlWq0OYUUr9qjYhxVHI1Jj8nj3hhzzveJZSsuyxBTi-mmxhxHlkEK0X1xPQrROttaDNHRdNCmZBL6Nz6az3z9-Wq8HZTQIqTdBOZn60Bpvkk1Aeg2sX9i57RMIJvVxIwFtGqus8Wp97_s8eANcSAlcWgn6hQFnx1n-dfP-1ubrCZ4ejafnINnWS-esb0En-8WVXKfnxZNGumRe7O6D4vvxh_PJp9Hsy8eTyXg2UoRRNoJ43hBFcGOgUkRLybjSRhOlJeGypEg1iiNS5rhUyWpJCUGUyQpzSXSDMT4o3m19u2G-MloZ30fpRBftSsa1CNKKfxVvF6INl4JVCOKSZoM3O4MYLoach1jZpIxz0pswJIEIInXNEOcZff0fugxDzJtnijFcEcLIwxQhlCJO683cb7eUijnfaJq7kWEpNu0Qm3aI23Zk-NX9Je_Qv3XIANwCV9aZ9QNW4vPk9HRr-gfDystY</recordid><startdate>202009</startdate><enddate>202009</enddate><creator>Lu, Jinwei</creator><creator>Ye, Chenyi</creator><creator>Huang, Yanyong</creator><creator>Huang, Donghui</creator><creator>Tang, Lan</creator><creator>Hou, Weiduo</creator><creator>Kuang, Zhihui</creator><creator>Chen, Yazhou</creator><creator>Xiao, Shining</creator><creator>Yishake, Mumingjiang</creator><creator>He, Rongxin</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5937-3878</orcidid></search><sort><creationdate>202009</creationdate><title>Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways</title><author>Lu, Jinwei ; Ye, Chenyi ; Huang, Yanyong ; Huang, Donghui ; Tang, Lan ; Hou, Weiduo ; Kuang, Zhihui ; Chen, Yazhou ; Xiao, Shining ; Yishake, Mumingjiang ; He, Rongxin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4767-13bf4c43fe1cc4daa78cded4cda48a062cfc8240111c079a644267a538a4df333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Actins - metabolism</topic><topic>AKT protein</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antioxidants</topic><topic>Bone loss</topic><topic>Bone Marrow Cells - drug effects</topic><topic>Bone Marrow Cells - metabolism</topic><topic>Bone resorption</topic><topic>Bone Resorption - pathology</topic><topic>Corilagin</topic><topic>Down-Regulation - drug effects</topic><topic>Estrogens</topic><topic>Estrogens - deficiency</topic><topic>Gene expression</topic><topic>Glucosides - chemistry</topic><topic>Glucosides - pharmacology</topic><topic>Hydrolyzable Tannins - chemistry</topic><topic>Hydrolyzable Tannins - pharmacology</topic><topic>Inflammation</topic><topic>Laboratory animals</topic><topic>Medicinal plants</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>NFATC Transcription Factors - metabolism</topic><topic>NF‐κB</topic><topic>Oophorectomy</topic><topic>Original</topic><topic>osteoclast</topic><topic>Osteoclastogenesis</topic><topic>Osteoclasts</topic><topic>Osteoclasts - drug effects</topic><topic>Osteoclasts - metabolism</topic><topic>Osteoclasts - pathology</topic><topic>Osteogenesis - drug effects</topic><topic>Osteoporosis</topic><topic>Osteoprotegerin - metabolism</topic><topic>Ovariectomy</topic><topic>Phosphatase</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>PI3K/AKT</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>RANK Ligand - pharmacology</topic><topic>RANKL</topic><topic>RAW 264.7 Cells</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>TRANCE protein</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Jinwei</creatorcontrib><creatorcontrib>Ye, Chenyi</creatorcontrib><creatorcontrib>Huang, Yanyong</creatorcontrib><creatorcontrib>Huang, Donghui</creatorcontrib><creatorcontrib>Tang, Lan</creatorcontrib><creatorcontrib>Hou, Weiduo</creatorcontrib><creatorcontrib>Kuang, Zhihui</creatorcontrib><creatorcontrib>Chen, Yazhou</creatorcontrib><creatorcontrib>Xiao, Shining</creatorcontrib><creatorcontrib>Yishake, Mumingjiang</creatorcontrib><creatorcontrib>He, Rongxin</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Jinwei</au><au>Ye, Chenyi</au><au>Huang, Yanyong</au><au>Huang, Donghui</au><au>Tang, Lan</au><au>Hou, Weiduo</au><au>Kuang, Zhihui</au><au>Chen, Yazhou</au><au>Xiao, Shining</au><au>Yishake, Mumingjiang</au><au>He, Rongxin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2020-09</date><risdate>2020</risdate><volume>24</volume><issue>18</issue><spage>10444</spage><epage>10457</epage><pages>10444-10457</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Over‐activated osteoclastogenesis, which is initiated by inflammation, has been implicated in osteoporosis. Corilagin, a natural compound extracted from various medicinal herbaceous plants, such as Cinnamomum cassia, has antioxidant and anti‐inflammatory activities. We found that Corilagin suppressed osteoclast differentiation in a dose‐dependent manner, significantly decreased osteoclast‐related gene expression and impaired bone resorption by osteoclasts. Moreover, phosphorylation of members of the nuclear factor‐kappaB (NF‐κB) and PI3K/AKT signalling pathways was reduced by Corilagin. In a murine model of osteoporosis, Corilagin inhibited osteoclast functions in vivo and restored oestrogen deficiency‐induced bone loss. In conclusion, our findings suggested that Corilagin inhibited osteoclastogenesis by down‐regulating the NF‐κB and PI3K/AKT signalling pathways, thus showing its potential possibility for the treatment of osteoporosis.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>32681612</pmid><doi>10.1111/jcmm.15657</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-5937-3878</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1582-1838 |
| ispartof | Journal of cellular and molecular medicine, 2020-09, Vol.24 (18), p.10444-10457 |
| issn | 1582-1838 1582-4934 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7521306 |
| source | MEDLINE; Wiley Online Library Open Access; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | 1-Phosphatidylinositol 3-kinase Actins - metabolism AKT protein Animal models Animals Antibodies Antioxidants Bone loss Bone Marrow Cells - drug effects Bone Marrow Cells - metabolism Bone resorption Bone Resorption - pathology Corilagin Down-Regulation - drug effects Estrogens Estrogens - deficiency Gene expression Glucosides - chemistry Glucosides - pharmacology Hydrolyzable Tannins - chemistry Hydrolyzable Tannins - pharmacology Inflammation Laboratory animals Medicinal plants Mice Mice, Inbred C57BL NF-kappa B - metabolism NF-κB protein NFATC Transcription Factors - metabolism NF‐κB Oophorectomy Original osteoclast Osteoclastogenesis Osteoclasts Osteoclasts - drug effects Osteoclasts - metabolism Osteoclasts - pathology Osteogenesis - drug effects Osteoporosis Osteoprotegerin - metabolism Ovariectomy Phosphatase Phosphatidylinositol 3-Kinases - metabolism Phosphorylation PI3K/AKT Proto-Oncogene Proteins c-akt - metabolism RANK Ligand - pharmacology RANKL RAW 264.7 Cells Reactive Oxygen Species - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Signal transduction Signal Transduction - drug effects TRANCE protein Tumor necrosis factor-TNF |
| title | Corilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T05%3A49%3A07IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Corilagin%20suppresses%20RANKL%E2%80%90induced%20osteoclastogenesis%20and%20inhibits%20oestrogen%20deficiency%E2%80%90induced%20bone%20loss%20via%20the%20NF%E2%80%90%CE%BAB%20and%20PI3K/AKT%20signalling%20pathways&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Lu,%20Jinwei&rft.date=2020-09&rft.volume=24&rft.issue=18&rft.spage=10444&rft.epage=10457&rft.pages=10444-10457&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.15657&rft_dat=%3Cproquest_pubme%3E2446628693%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2446628693&rft_id=info:pmid/32681612&rfr_iscdi=true |