Cytisine attenuates bone loss of ovariectomy mouse by preventing RANKL‐induced osteoclastogenesis
Postmenopausal Osteoporosis (PMOP) is oestrogen withdrawal characterized of much production and activation by osteoclast in the elderly female. Cytisine is a quinolizidine alkaloid that comes from seeds or other plants of the Leguminosae (Fabaceae) family. Cytisine has been shown several potential p...
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| creator | Qian, Zhi Zhong, Zeyuan Ni, Shuo Li, Dejian Zhang, Fangxue Zhou, Ying Kang, Zhanrong Qian, Jun Yu, Baoqing |
| description | Postmenopausal Osteoporosis (PMOP) is oestrogen withdrawal characterized of much production and activation by osteoclast in the elderly female. Cytisine is a quinolizidine alkaloid that comes from seeds or other plants of the Leguminosae (Fabaceae) family. Cytisine has been shown several potential pharmacological functions. However, its effects on PMOP remain unknown. This study designed to explore whether Cytisine is able to suppress RANKL‐induced osteoclastogenesis and prevent the bone loss induced by oestrogen deficiency in ovariectomized (OVX) mice. In this study, we investigated the effect of Cytisine on RAW 264.7 cells and bone marrow monocytes (BMMs) derived osteoclast culture system in vitro and observed the effect of Cytisine on ovariectomized (OVX) mice model to imitate postmenopausal osteoporosis in vivo. We found that Cytisine inhibited F‐actin ring formation and tartrate‐resistant acid phosphatase (TRAP) staining in dose‐dependent ways, as well as bone resorption by pit formation assays. For molecular mechanism, Cytisine suppressed RANK‐related trigger RANKL by phosphorylation JNK/ERK/p38‐MAPK, IκBα/p65‐NF‐κB, and PI3K/AKT axis and significantly inhibited these signalling pathways. However, the suppression of PI3K‐AKT‐NFATc1 axis was rescued by AKT activator SC79. Meanwhile, Cytisine inhibited RANKL‐induced RANK‐TRAF6 association and RANKL‐related gene and protein markers such as NFATc1, Cathepsin K, MMP‐9 and TRAP. Our study indicated that Cytisine could suppress bone loss in OVX mouse through inhibited osteoclastogenesis. All data provide the evidence that Cytisine may be a promising agent in the treatment of osteoclast‐related diseases such as osteoporosis. |
| doi_str_mv | 10.1111/jcmm.15622 |
| format | Article |
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Cytisine is a quinolizidine alkaloid that comes from seeds or other plants of the Leguminosae (Fabaceae) family. Cytisine has been shown several potential pharmacological functions. However, its effects on PMOP remain unknown. This study designed to explore whether Cytisine is able to suppress RANKL‐induced osteoclastogenesis and prevent the bone loss induced by oestrogen deficiency in ovariectomized (OVX) mice. In this study, we investigated the effect of Cytisine on RAW 264.7 cells and bone marrow monocytes (BMMs) derived osteoclast culture system in vitro and observed the effect of Cytisine on ovariectomized (OVX) mice model to imitate postmenopausal osteoporosis in vivo. We found that Cytisine inhibited F‐actin ring formation and tartrate‐resistant acid phosphatase (TRAP) staining in dose‐dependent ways, as well as bone resorption by pit formation assays. For molecular mechanism, Cytisine suppressed RANK‐related trigger RANKL by phosphorylation JNK/ERK/p38‐MAPK, IκBα/p65‐NF‐κB, and PI3K/AKT axis and significantly inhibited these signalling pathways. However, the suppression of PI3K‐AKT‐NFATc1 axis was rescued by AKT activator SC79. Meanwhile, Cytisine inhibited RANKL‐induced RANK‐TRAF6 association and RANKL‐related gene and protein markers such as NFATc1, Cathepsin K, MMP‐9 and TRAP. Our study indicated that Cytisine could suppress bone loss in OVX mouse through inhibited osteoclastogenesis. All data provide the evidence that Cytisine may be a promising agent in the treatment of osteoclast‐related diseases such as osteoporosis.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.15622</identifier><identifier>PMID: 32790170</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; Acid phosphatase (tartrate-resistant) ; Acids ; Actin ; AKT protein ; AKT‐NFATc1 ; Alkaloids - metabolism ; Animals ; Antibiotics ; Antibodies ; Azocines - metabolism ; Bone growth ; Bone loss ; Bone marrow ; Bone resorption ; Bone Resorption - metabolism ; Cathepsin K ; Cell culture ; cytisine ; Cytokines ; Estrogens ; Female ; Kinases ; Laboratory animals ; MAP kinase ; MAPK ; Mice ; Mice, Inbred C57BL ; Mineralization ; Monocytes ; NF-kappa B - metabolism ; NF‐κB ; Oophorectomy ; Original ; Osteoclastogenesis ; Osteoclasts - metabolism ; Osteogenesis - physiology ; Osteoporosis ; Ovariectomy ; Ovariectomy - methods ; Phosphatase ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Post-menopause ; Proto-Oncogene Proteins c-akt - metabolism ; Quinolizines - metabolism ; RANK Ligand - metabolism ; RAW 264.7 Cells ; SC79 ; Seeds ; Signal transduction ; Signal Transduction - physiology ; TRAF6 protein ; TRANCE protein ; Tumor necrosis factor-TNF</subject><ispartof>Journal of cellular and molecular medicine, 2020-09, Vol.24 (17), p.10112-10127</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-c4482-d836ceaf166cee2e36a55355e8b6c23a0e40ceb58e83d451b07a8f90f77510d33</citedby><cites>FETCH-LOGICAL-c4482-d836ceaf166cee2e36a55355e8b6c23a0e40ceb58e83d451b07a8f90f77510d33</cites><orcidid>0000-0003-3265-7560</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/PMC7520284/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7520284/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1416,11561,27923,27924,45573,45574,46051,46475,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32790170$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qian, Zhi</creatorcontrib><creatorcontrib>Zhong, Zeyuan</creatorcontrib><creatorcontrib>Ni, Shuo</creatorcontrib><creatorcontrib>Li, Dejian</creatorcontrib><creatorcontrib>Zhang, Fangxue</creatorcontrib><creatorcontrib>Zhou, Ying</creatorcontrib><creatorcontrib>Kang, Zhanrong</creatorcontrib><creatorcontrib>Qian, Jun</creatorcontrib><creatorcontrib>Yu, Baoqing</creatorcontrib><title>Cytisine attenuates bone loss of ovariectomy mouse by preventing RANKL‐induced osteoclastogenesis</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Postmenopausal Osteoporosis (PMOP) is oestrogen withdrawal characterized of much production and activation by osteoclast in the elderly female. Cytisine is a quinolizidine alkaloid that comes from seeds or other plants of the Leguminosae (Fabaceae) family. Cytisine has been shown several potential pharmacological functions. However, its effects on PMOP remain unknown. This study designed to explore whether Cytisine is able to suppress RANKL‐induced osteoclastogenesis and prevent the bone loss induced by oestrogen deficiency in ovariectomized (OVX) mice. In this study, we investigated the effect of Cytisine on RAW 264.7 cells and bone marrow monocytes (BMMs) derived osteoclast culture system in vitro and observed the effect of Cytisine on ovariectomized (OVX) mice model to imitate postmenopausal osteoporosis in vivo. We found that Cytisine inhibited F‐actin ring formation and tartrate‐resistant acid phosphatase (TRAP) staining in dose‐dependent ways, as well as bone resorption by pit formation assays. For molecular mechanism, Cytisine suppressed RANK‐related trigger RANKL by phosphorylation JNK/ERK/p38‐MAPK, IκBα/p65‐NF‐κB, and PI3K/AKT axis and significantly inhibited these signalling pathways. However, the suppression of PI3K‐AKT‐NFATc1 axis was rescued by AKT activator SC79. Meanwhile, Cytisine inhibited RANKL‐induced RANK‐TRAF6 association and RANKL‐related gene and protein markers such as NFATc1, Cathepsin K, MMP‐9 and TRAP. Our study indicated that Cytisine could suppress bone loss in OVX mouse through inhibited osteoclastogenesis. All data provide the evidence that Cytisine may be a promising agent in the treatment of osteoclast‐related diseases such as osteoporosis.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Acid phosphatase (tartrate-resistant)</subject><subject>Acids</subject><subject>Actin</subject><subject>AKT protein</subject><subject>AKT‐NFATc1</subject><subject>Alkaloids - metabolism</subject><subject>Animals</subject><subject>Antibiotics</subject><subject>Antibodies</subject><subject>Azocines - metabolism</subject><subject>Bone growth</subject><subject>Bone loss</subject><subject>Bone marrow</subject><subject>Bone resorption</subject><subject>Bone Resorption - metabolism</subject><subject>Cathepsin K</subject><subject>Cell culture</subject><subject>cytisine</subject><subject>Cytokines</subject><subject>Estrogens</subject><subject>Female</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>MAP kinase</subject><subject>MAPK</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mineralization</subject><subject>Monocytes</subject><subject>NF-kappa B - metabolism</subject><subject>NF‐κB</subject><subject>Oophorectomy</subject><subject>Original</subject><subject>Osteoclastogenesis</subject><subject>Osteoclasts - metabolism</subject><subject>Osteogenesis - physiology</subject><subject>Osteoporosis</subject><subject>Ovariectomy</subject><subject>Ovariectomy - methods</subject><subject>Phosphatase</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Post-menopause</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Quinolizines - metabolism</subject><subject>RANK Ligand - metabolism</subject><subject>RAW 264.7 Cells</subject><subject>SC79</subject><subject>Seeds</subject><subject>Signal transduction</subject><subject>Signal Transduction - physiology</subject><subject>TRAF6 protein</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>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU1uFDEQhS1EREJgwwGQJTYIaYJ_u90bpGjET8IEJARry-2uHjzqtie2e1DvOAJn5CQ4mSECFtSmquRPT6_8EHpCyRkt9XJjx_GMyoqxe-iESsUWouHi_mGmiqtj9DClDSG8orx5gI45qxtCa3KC7HLOLjkP2OQMfjIZEm5D2YeQEg49DjsTHdgcxhmPYUqA2xlvI-zAZ-fX-NP5h_ern99_ON9NFjocUoZgB5NyWIOH5NIjdNSbIcHjQz9FX968_rx8t1h9fHuxPF8trBDFaKd4ZcH0tCoNGPDKSMmlBNVWlnFDQBALrVSgeCckbUltVN-Qvq4lJR3np-jVXnc7tSN0thiMZtDb6EYTZx2M03-_ePdVr8NO15IRpkQReH4QiOF6gpT16JKFYTAeyuWaCS6IlDVtCvrsH3QTpujLeYUSlaCMclKoF3vKxvKbEfo7M5Tom-z0TXb6NrsCP_3T_h36O6wC0D3wzQ0w_0dKXy6vrvaivwA5hadr</recordid><startdate>202009</startdate><enddate>202009</enddate><creator>Qian, Zhi</creator><creator>Zhong, Zeyuan</creator><creator>Ni, Shuo</creator><creator>Li, Dejian</creator><creator>Zhang, Fangxue</creator><creator>Zhou, Ying</creator><creator>Kang, Zhanrong</creator><creator>Qian, Jun</creator><creator>Yu, Baoqing</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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/0000-0003-3265-7560</orcidid></search><sort><creationdate>202009</creationdate><title>Cytisine attenuates bone loss of ovariectomy mouse by preventing RANKL‐induced osteoclastogenesis</title><author>Qian, Zhi ; Zhong, Zeyuan ; Ni, Shuo ; Li, Dejian ; Zhang, Fangxue ; Zhou, Ying ; Kang, Zhanrong ; Qian, Jun ; Yu, Baoqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4482-d836ceaf166cee2e36a55355e8b6c23a0e40ceb58e83d451b07a8f90f77510d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Acid phosphatase (tartrate-resistant)</topic><topic>Acids</topic><topic>Actin</topic><topic>AKT protein</topic><topic>AKT‐NFATc1</topic><topic>Alkaloids - metabolism</topic><topic>Animals</topic><topic>Antibiotics</topic><topic>Antibodies</topic><topic>Azocines - metabolism</topic><topic>Bone growth</topic><topic>Bone loss</topic><topic>Bone marrow</topic><topic>Bone resorption</topic><topic>Bone Resorption - metabolism</topic><topic>Cathepsin K</topic><topic>Cell culture</topic><topic>cytisine</topic><topic>Cytokines</topic><topic>Estrogens</topic><topic>Female</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>MAP kinase</topic><topic>MAPK</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mineralization</topic><topic>Monocytes</topic><topic>NF-kappa B - metabolism</topic><topic>NF‐κB</topic><topic>Oophorectomy</topic><topic>Original</topic><topic>Osteoclastogenesis</topic><topic>Osteoclasts - metabolism</topic><topic>Osteogenesis - physiology</topic><topic>Osteoporosis</topic><topic>Ovariectomy</topic><topic>Ovariectomy - methods</topic><topic>Phosphatase</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Post-menopause</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Quinolizines - metabolism</topic><topic>RANK Ligand - metabolism</topic><topic>RAW 264.7 Cells</topic><topic>SC79</topic><topic>Seeds</topic><topic>Signal transduction</topic><topic>Signal Transduction - physiology</topic><topic>TRAF6 protein</topic><topic>TRANCE protein</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qian, Zhi</creatorcontrib><creatorcontrib>Zhong, Zeyuan</creatorcontrib><creatorcontrib>Ni, Shuo</creatorcontrib><creatorcontrib>Li, Dejian</creatorcontrib><creatorcontrib>Zhang, Fangxue</creatorcontrib><creatorcontrib>Zhou, Ying</creatorcontrib><creatorcontrib>Kang, Zhanrong</creatorcontrib><creatorcontrib>Qian, Jun</creatorcontrib><creatorcontrib>Yu, Baoqing</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</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>Qian, Zhi</au><au>Zhong, Zeyuan</au><au>Ni, Shuo</au><au>Li, Dejian</au><au>Zhang, Fangxue</au><au>Zhou, Ying</au><au>Kang, Zhanrong</au><au>Qian, Jun</au><au>Yu, Baoqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytisine attenuates bone loss of ovariectomy mouse by preventing RANKL‐induced osteoclastogenesis</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>17</issue><spage>10112</spage><epage>10127</epage><pages>10112-10127</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Postmenopausal Osteoporosis (PMOP) is oestrogen withdrawal characterized of much production and activation by osteoclast in the elderly female. Cytisine is a quinolizidine alkaloid that comes from seeds or other plants of the Leguminosae (Fabaceae) family. Cytisine has been shown several potential pharmacological functions. However, its effects on PMOP remain unknown. This study designed to explore whether Cytisine is able to suppress RANKL‐induced osteoclastogenesis and prevent the bone loss induced by oestrogen deficiency in ovariectomized (OVX) mice. In this study, we investigated the effect of Cytisine on RAW 264.7 cells and bone marrow monocytes (BMMs) derived osteoclast culture system in vitro and observed the effect of Cytisine on ovariectomized (OVX) mice model to imitate postmenopausal osteoporosis in vivo. We found that Cytisine inhibited F‐actin ring formation and tartrate‐resistant acid phosphatase (TRAP) staining in dose‐dependent ways, as well as bone resorption by pit formation assays. For molecular mechanism, Cytisine suppressed RANK‐related trigger RANKL by phosphorylation JNK/ERK/p38‐MAPK, IκBα/p65‐NF‐κB, and PI3K/AKT axis and significantly inhibited these signalling pathways. However, the suppression of PI3K‐AKT‐NFATc1 axis was rescued by AKT activator SC79. Meanwhile, Cytisine inhibited RANKL‐induced RANK‐TRAF6 association and RANKL‐related gene and protein markers such as NFATc1, Cathepsin K, MMP‐9 and TRAP. Our study indicated that Cytisine could suppress bone loss in OVX mouse through inhibited osteoclastogenesis. All data provide the evidence that Cytisine may be a promising agent in the treatment of osteoclast‐related diseases such as osteoporosis.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>32790170</pmid><doi>10.1111/jcmm.15622</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0003-3265-7560</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase Acid phosphatase (tartrate-resistant) Acids Actin AKT protein AKT‐NFATc1 Alkaloids - metabolism Animals Antibiotics Antibodies Azocines - metabolism Bone growth Bone loss Bone marrow Bone resorption Bone Resorption - metabolism Cathepsin K Cell culture cytisine Cytokines Estrogens Female Kinases Laboratory animals MAP kinase MAPK Mice Mice, Inbred C57BL Mineralization Monocytes NF-kappa B - metabolism NF‐κB Oophorectomy Original Osteoclastogenesis Osteoclasts - metabolism Osteogenesis - physiology Osteoporosis Ovariectomy Ovariectomy - methods Phosphatase Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Post-menopause Proto-Oncogene Proteins c-akt - metabolism Quinolizines - metabolism RANK Ligand - metabolism RAW 264.7 Cells SC79 Seeds Signal transduction Signal Transduction - physiology TRAF6 protein TRANCE protein Tumor necrosis factor-TNF |
| title | Cytisine attenuates bone loss of ovariectomy mouse by preventing RANKL‐induced osteoclastogenesis |
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