Triptolide inhibits the function of TNF-α in osteoblast differentiation by inhibiting the NF-κB signaling pathway
Chronic inflammation often delays fracture healing or leads to bone nonunion. Effectively suppressing pathological inflammation is crucial for fracture healing or bone remodeling. Triptolide, which is a diterpenoid epoxide, is the major active component of the Thunder God Vine, Tripterygium wilfordi...
Gespeichert in:
| Veröffentlicht in: | Experimental and therapeutic medicine 2017-09, Vol.14 (3), p.2235-2240 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2240 |
|---|---|
| container_issue | 3 |
| container_start_page | 2235 |
| container_title | Experimental and therapeutic medicine |
| container_volume | 14 |
| creator | Liu, Shen-Peng Wang, Guo-Dong Du, Xue-Jun Wan, Guang Wu, Jun-Tao Miao, Lian-Bao Liang, Qiu-Dong |
| description | Chronic inflammation often delays fracture healing or leads to bone nonunion. Effectively suppressing pathological inflammation is crucial for fracture healing or bone remodeling. Triptolide, which is a diterpenoid epoxide, is the major active component of the Thunder God Vine, Tripterygium wilfordii. The aim of the present study was to investigate the role of triptolide in osteoblast differentiation and explore the molecular mechanisms of triptolide in fracture healing. Alkaline phosphatase (ALP) activity was used to evaluate osteoblast differentiation. ALP activity was measured via histochemical staining and western blotting was used to determine the expression of factors associated with inflammation. C2C12 cells were initially treated with 200 ng/ml bone morphogenetic protein (BMP)-2 alone for 3 days, which caused a significant increase in ALP activity (P |
| doi_str_mv | 10.3892/etm.2017.4749 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5609201</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1945221429</sourcerecordid><originalsourceid>FETCH-LOGICAL-c445t-a22b989bbef38bba258ef999e185aab15de6bd413b02f1b430d89afde4c443343</originalsourceid><addsrcrecordid>eNpdkc9uEzEQxi0EolXbI1e0EkLisqn_JvYFiVYtIJVyCWfLXtuJq4292F5QHosrD8Ez4U3SCGofPPL85tPMfAC8QnBGuMCXtmxmGKLFjC6oeAZO0ULgFkHEnh9iKDg6ARc5P8B62Bxxzl6CE8zFHCPKT0FeJj-U2HtjGx_WXvuSm7K2jRtDV3wMTXTN8v62_fOr5puYi426V7k0xjtnkw3Fqx2nt48CPqx2ElPV76sm-1VQ_fQ5qLL-qbbn4IVTfbYXh_cMfLu9WV5_au--fvx8_eGu7ShlpVUYa8GF1tYRrrXCjFsnhLCIM6U0YsbOtaGIaIgd0pRAw4VyxtJaTwglZ-D9XncY9caarvaaVC-H5DcqbWVUXv6fCX4tV_GHZHMo6lqrwLuDQIrfR5uL3Pjc2b5XwcYxSyQow3WPWFT0zRP0IY6pzr2jMGKEQFKpdk91KeacrDs2g6CcHJXVUTk5KidHK__63wmO9KN_FXi7B_KggvEm5iNzs_zSwnp3Qn8B1FWsNA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1942153303</pqid></control><display><type>article</type><title>Triptolide inhibits the function of TNF-α in osteoblast differentiation by inhibiting the NF-κB signaling pathway</title><source>PubMed Central</source><creator>Liu, Shen-Peng ; Wang, Guo-Dong ; Du, Xue-Jun ; Wan, Guang ; Wu, Jun-Tao ; Miao, Lian-Bao ; Liang, Qiu-Dong</creator><creatorcontrib>Liu, Shen-Peng ; Wang, Guo-Dong ; Du, Xue-Jun ; Wan, Guang ; Wu, Jun-Tao ; Miao, Lian-Bao ; Liang, Qiu-Dong</creatorcontrib><description>Chronic inflammation often delays fracture healing or leads to bone nonunion. Effectively suppressing pathological inflammation is crucial for fracture healing or bone remodeling. Triptolide, which is a diterpenoid epoxide, is the major active component of the Thunder God Vine, Tripterygium wilfordii. The aim of the present study was to investigate the role of triptolide in osteoblast differentiation and explore the molecular mechanisms of triptolide in fracture healing. Alkaline phosphatase (ALP) activity was used to evaluate osteoblast differentiation. ALP activity was measured via histochemical staining and western blotting was used to determine the expression of factors associated with inflammation. C2C12 cells were initially treated with 200 ng/ml bone morphogenetic protein (BMP)-2 alone for 3 days, which caused a significant increase in ALP activity (P<0.01). However, treatment with tumor necrosis factor (TNF)-α significantly decreased the ALP activity (P<0.05). Notably, treatment with the chronic inflammatory cytokine TNF-α significantly decreased the effect of BMP-2 in C2C12 cells compared with BMP-2 treatment alone (P<0.01). C2C12 cells were treated with increasing concentrations of BMP-2 or TNF-α for 3 days. The results demonstrated that TNF-α treatment significantly inhibited BMP-2-induced osteoblast differentiation in a dose-dependent manner (P<0.01). The role of triptolide in BMP-2-induced osteoblast differentiation was also examined. Cells were treated with BMP-2, BMP-2 + TNF-α alone, or BMP2 + TNF-α with increasing concentrations of triptolide (4, 8 or 16 ng/ml). After 3 days, the results of ALP activity revealed that triptolide significantly reversed the TNF-α-associated inhibition of osteoblast differentiation (P<0.01). Western blotting analysis demonstrated that triptolide markedly inhibited the phosphorylation of nuclear factor-κB, therefore suppressing the effects of TNF-α. In summary, triptolide is able to reverse the TNF-α-associated suppression of osteoblast differentiation, suggesting that triptolide treatment may have a positive effect on bone remodeling and fracture repairing.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2017.4749</identifier><identifier>PMID: 28962148</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>bone morphogenetic protein-1 ; Cytokines ; fracture healing ; Gene expression ; Inflammation ; Kinases ; osteoblast differentiation ; Physiology ; Proteins ; Rheumatoid arthritis ; Stem cells ; Studies ; triptolide ; Tumor necrosis factor-TNF</subject><ispartof>Experimental and therapeutic medicine, 2017-09, Vol.14 (3), p.2235-2240</ispartof><rights>Copyright © 2017, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright © 2017, Spandidos Publications 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-a22b989bbef38bba258ef999e185aab15de6bd413b02f1b430d89afde4c443343</citedby><cites>FETCH-LOGICAL-c445t-a22b989bbef38bba258ef999e185aab15de6bd413b02f1b430d89afde4c443343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609201/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609201/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28962148$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Shen-Peng</creatorcontrib><creatorcontrib>Wang, Guo-Dong</creatorcontrib><creatorcontrib>Du, Xue-Jun</creatorcontrib><creatorcontrib>Wan, Guang</creatorcontrib><creatorcontrib>Wu, Jun-Tao</creatorcontrib><creatorcontrib>Miao, Lian-Bao</creatorcontrib><creatorcontrib>Liang, Qiu-Dong</creatorcontrib><title>Triptolide inhibits the function of TNF-α in osteoblast differentiation by inhibiting the NF-κB signaling pathway</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>Chronic inflammation often delays fracture healing or leads to bone nonunion. Effectively suppressing pathological inflammation is crucial for fracture healing or bone remodeling. Triptolide, which is a diterpenoid epoxide, is the major active component of the Thunder God Vine, Tripterygium wilfordii. The aim of the present study was to investigate the role of triptolide in osteoblast differentiation and explore the molecular mechanisms of triptolide in fracture healing. Alkaline phosphatase (ALP) activity was used to evaluate osteoblast differentiation. ALP activity was measured via histochemical staining and western blotting was used to determine the expression of factors associated with inflammation. C2C12 cells were initially treated with 200 ng/ml bone morphogenetic protein (BMP)-2 alone for 3 days, which caused a significant increase in ALP activity (P<0.01). However, treatment with tumor necrosis factor (TNF)-α significantly decreased the ALP activity (P<0.05). Notably, treatment with the chronic inflammatory cytokine TNF-α significantly decreased the effect of BMP-2 in C2C12 cells compared with BMP-2 treatment alone (P<0.01). C2C12 cells were treated with increasing concentrations of BMP-2 or TNF-α for 3 days. The results demonstrated that TNF-α treatment significantly inhibited BMP-2-induced osteoblast differentiation in a dose-dependent manner (P<0.01). The role of triptolide in BMP-2-induced osteoblast differentiation was also examined. Cells were treated with BMP-2, BMP-2 + TNF-α alone, or BMP2 + TNF-α with increasing concentrations of triptolide (4, 8 or 16 ng/ml). After 3 days, the results of ALP activity revealed that triptolide significantly reversed the TNF-α-associated inhibition of osteoblast differentiation (P<0.01). Western blotting analysis demonstrated that triptolide markedly inhibited the phosphorylation of nuclear factor-κB, therefore suppressing the effects of TNF-α. In summary, triptolide is able to reverse the TNF-α-associated suppression of osteoblast differentiation, suggesting that triptolide treatment may have a positive effect on bone remodeling and fracture repairing.</description><subject>bone morphogenetic protein-1</subject><subject>Cytokines</subject><subject>fracture healing</subject><subject>Gene expression</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>osteoblast differentiation</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Rheumatoid arthritis</subject><subject>Stem cells</subject><subject>Studies</subject><subject>triptolide</subject><subject>Tumor necrosis factor-TNF</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpdkc9uEzEQxi0EolXbI1e0EkLisqn_JvYFiVYtIJVyCWfLXtuJq4292F5QHosrD8Ez4U3SCGofPPL85tPMfAC8QnBGuMCXtmxmGKLFjC6oeAZO0ULgFkHEnh9iKDg6ARc5P8B62Bxxzl6CE8zFHCPKT0FeJj-U2HtjGx_WXvuSm7K2jRtDV3wMTXTN8v62_fOr5puYi426V7k0xjtnkw3Fqx2nt48CPqx2ElPV76sm-1VQ_fQ5qLL-qbbn4IVTfbYXh_cMfLu9WV5_au--fvx8_eGu7ShlpVUYa8GF1tYRrrXCjFsnhLCIM6U0YsbOtaGIaIgd0pRAw4VyxtJaTwglZ-D9XncY9caarvaaVC-H5DcqbWVUXv6fCX4tV_GHZHMo6lqrwLuDQIrfR5uL3Pjc2b5XwcYxSyQow3WPWFT0zRP0IY6pzr2jMGKEQFKpdk91KeacrDs2g6CcHJXVUTk5KidHK__63wmO9KN_FXi7B_KggvEm5iNzs_zSwnp3Qn8B1FWsNA</recordid><startdate>20170901</startdate><enddate>20170901</enddate><creator>Liu, Shen-Peng</creator><creator>Wang, Guo-Dong</creator><creator>Du, Xue-Jun</creator><creator>Wan, Guang</creator><creator>Wu, Jun-Tao</creator><creator>Miao, Lian-Bao</creator><creator>Liang, Qiu-Dong</creator><general>D.A. Spandidos</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170901</creationdate><title>Triptolide inhibits the function of TNF-α in osteoblast differentiation by inhibiting the NF-κB signaling pathway</title><author>Liu, Shen-Peng ; Wang, Guo-Dong ; Du, Xue-Jun ; Wan, Guang ; Wu, Jun-Tao ; Miao, Lian-Bao ; Liang, Qiu-Dong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-a22b989bbef38bba258ef999e185aab15de6bd413b02f1b430d89afde4c443343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>bone morphogenetic protein-1</topic><topic>Cytokines</topic><topic>fracture healing</topic><topic>Gene expression</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>osteoblast differentiation</topic><topic>Physiology</topic><topic>Proteins</topic><topic>Rheumatoid arthritis</topic><topic>Stem cells</topic><topic>Studies</topic><topic>triptolide</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Shen-Peng</creatorcontrib><creatorcontrib>Wang, Guo-Dong</creatorcontrib><creatorcontrib>Du, Xue-Jun</creatorcontrib><creatorcontrib>Wan, Guang</creatorcontrib><creatorcontrib>Wu, Jun-Tao</creatorcontrib><creatorcontrib>Miao, Lian-Bao</creatorcontrib><creatorcontrib>Liang, Qiu-Dong</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Experimental and therapeutic medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Shen-Peng</au><au>Wang, Guo-Dong</au><au>Du, Xue-Jun</au><au>Wan, Guang</au><au>Wu, Jun-Tao</au><au>Miao, Lian-Bao</au><au>Liang, Qiu-Dong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Triptolide inhibits the function of TNF-α in osteoblast differentiation by inhibiting the NF-κB signaling pathway</atitle><jtitle>Experimental and therapeutic medicine</jtitle><addtitle>Exp Ther Med</addtitle><date>2017-09-01</date><risdate>2017</risdate><volume>14</volume><issue>3</issue><spage>2235</spage><epage>2240</epage><pages>2235-2240</pages><issn>1792-0981</issn><eissn>1792-1015</eissn><abstract>Chronic inflammation often delays fracture healing or leads to bone nonunion. Effectively suppressing pathological inflammation is crucial for fracture healing or bone remodeling. Triptolide, which is a diterpenoid epoxide, is the major active component of the Thunder God Vine, Tripterygium wilfordii. The aim of the present study was to investigate the role of triptolide in osteoblast differentiation and explore the molecular mechanisms of triptolide in fracture healing. Alkaline phosphatase (ALP) activity was used to evaluate osteoblast differentiation. ALP activity was measured via histochemical staining and western blotting was used to determine the expression of factors associated with inflammation. C2C12 cells were initially treated with 200 ng/ml bone morphogenetic protein (BMP)-2 alone for 3 days, which caused a significant increase in ALP activity (P<0.01). However, treatment with tumor necrosis factor (TNF)-α significantly decreased the ALP activity (P<0.05). Notably, treatment with the chronic inflammatory cytokine TNF-α significantly decreased the effect of BMP-2 in C2C12 cells compared with BMP-2 treatment alone (P<0.01). C2C12 cells were treated with increasing concentrations of BMP-2 or TNF-α for 3 days. The results demonstrated that TNF-α treatment significantly inhibited BMP-2-induced osteoblast differentiation in a dose-dependent manner (P<0.01). The role of triptolide in BMP-2-induced osteoblast differentiation was also examined. Cells were treated with BMP-2, BMP-2 + TNF-α alone, or BMP2 + TNF-α with increasing concentrations of triptolide (4, 8 or 16 ng/ml). After 3 days, the results of ALP activity revealed that triptolide significantly reversed the TNF-α-associated inhibition of osteoblast differentiation (P<0.01). Western blotting analysis demonstrated that triptolide markedly inhibited the phosphorylation of nuclear factor-κB, therefore suppressing the effects of TNF-α. In summary, triptolide is able to reverse the TNF-α-associated suppression of osteoblast differentiation, suggesting that triptolide treatment may have a positive effect on bone remodeling and fracture repairing.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28962148</pmid><doi>10.3892/etm.2017.4749</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1792-0981 |
| ispartof | Experimental and therapeutic medicine, 2017-09, Vol.14 (3), p.2235-2240 |
| issn | 1792-0981 1792-1015 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5609201 |
| source | PubMed Central |
| subjects | bone morphogenetic protein-1 Cytokines fracture healing Gene expression Inflammation Kinases osteoblast differentiation Physiology Proteins Rheumatoid arthritis Stem cells Studies triptolide Tumor necrosis factor-TNF |
| title | Triptolide inhibits the function of TNF-α in osteoblast differentiation by inhibiting the NF-κB signaling pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-15T14%3A54%3A42IST&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=Triptolide%20inhibits%20the%20function%20of%20TNF-%CE%B1%20in%20osteoblast%20differentiation%20by%20inhibiting%20the%20NF-%CE%BAB%20signaling%20pathway&rft.jtitle=Experimental%20and%20therapeutic%20medicine&rft.au=Liu,%20Shen-Peng&rft.date=2017-09-01&rft.volume=14&rft.issue=3&rft.spage=2235&rft.epage=2240&rft.pages=2235-2240&rft.issn=1792-0981&rft.eissn=1792-1015&rft_id=info:doi/10.3892/etm.2017.4749&rft_dat=%3Cproquest_pubme%3E1945221429%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=1942153303&rft_id=info:pmid/28962148&rfr_iscdi=true |