Polydatin suppresses nucleus pulposus cell senescence, promotes matrix homeostasis and attenuates intervertebral disc degeneration in rats
Intervertebral disc degeneration (IVDD) is one of the major causes of low back pain. Polydatin (PD) has been shown to exert multiple pharmacological effects on different diseases; here, we test the therapeutic potential of PD for IVDD. In in‐vitro experiments, we confirmed PD is nontoxic to nucleus...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2018-11, Vol.22 (11), p.5720-5731 |
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| creator | Wang, Jianle Huang, Chongan Lin, Zongze Pan, Xiangxiang Chen, Jiaoxiang Zheng, Gang Tian, Naifeng Yan, Yingzhao Zhang, Zengjie Hu, Jianing Cheng, Pu Wang, Xiangyang Zhang, Xiaolei |
| description | Intervertebral disc degeneration (IVDD) is one of the major causes of low back pain. Polydatin (PD) has been shown to exert multiple pharmacological effects on different diseases; here, we test the therapeutic potential of PD for IVDD. In in‐vitro experiments, we confirmed PD is nontoxic to nucleus pulposus cells (NPCs) under the concentration of 400 μmol/L. Furthermore, PD was able to decrease the level of senescence in TNF‐α‐treated NPCs, as indicated by β‐gal staining as well as senescence markers p53 and p16 expression. In the aspect of extracellular matrix (ECM), PD not only reduced metalloproteinase 3 (MMP‐3), metalloproteinase 13 (MMP‐13) and a disintegrin‐like and metalloproteinase thrombospondin type 1 motif 4 (ADAMTS‐4) expression, but also increased aggrecan and collagen II levels. Mitochondrion is closely related to cellular senescence and ECM homeostasis; mechanistically, we found PD may rescue TNF‐α‐induced mitochondrial dysfunction, and it may also promote Nrf2 expression and activity. Silencing Nrf2 partly abolished the protective effects of PD on mitochondrial homeostasis, senescence and ECM homeostasis in TNF‐α‐treated NPCs. Correspondingly, PD ameliorated IVDD in rat model by promoting Nrf2 activity, preserving ECM and inhibiting senescence in nucleus pulposus cells. To sum up, our study suggests that PD exerts protective effects in NPCs against IVDD and reveals the underlying mechanism of PD on Nrf2 activation in NPCs. |
| doi_str_mv | 10.1111/jcmm.13848 |
| format | Article |
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Polydatin (PD) has been shown to exert multiple pharmacological effects on different diseases; here, we test the therapeutic potential of PD for IVDD. In in‐vitro experiments, we confirmed PD is nontoxic to nucleus pulposus cells (NPCs) under the concentration of 400 μmol/L. Furthermore, PD was able to decrease the level of senescence in TNF‐α‐treated NPCs, as indicated by β‐gal staining as well as senescence markers p53 and p16 expression. In the aspect of extracellular matrix (ECM), PD not only reduced metalloproteinase 3 (MMP‐3), metalloproteinase 13 (MMP‐13) and a disintegrin‐like and metalloproteinase thrombospondin type 1 motif 4 (ADAMTS‐4) expression, but also increased aggrecan and collagen II levels. Mitochondrion is closely related to cellular senescence and ECM homeostasis; mechanistically, we found PD may rescue TNF‐α‐induced mitochondrial dysfunction, and it may also promote Nrf2 expression and activity. Silencing Nrf2 partly abolished the protective effects of PD on mitochondrial homeostasis, senescence and ECM homeostasis in TNF‐α‐treated NPCs. Correspondingly, PD ameliorated IVDD in rat model by promoting Nrf2 activity, preserving ECM and inhibiting senescence in nucleus pulposus cells. To sum up, our study suggests that PD exerts protective effects in NPCs against IVDD and reveals the underlying mechanism of PD on Nrf2 activation in NPCs.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.13848</identifier><identifier>PMID: 30358118</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>ADAMTS4 Protein - genetics ; Aggrecan ; Aggrecans - genetics ; Animals ; Cells, Cultured ; Cellular Senescence - drug effects ; Collagen (type II) ; Collagen - genetics ; Degeneration ; Disease Models, Animal ; Extracellular matrix ; Extracellular Matrix - drug effects ; Extracellular Matrix - genetics ; Glucosides - pharmacology ; Homeostasis ; Humans ; Intervertebral Disc - drug effects ; Intervertebral Disc - pathology ; intervertebral disc degeneration ; Intervertebral Disc Degeneration - drug therapy ; Intervertebral Disc Degeneration - genetics ; Intervertebral Disc Degeneration - pathology ; Intervertebral discs ; Low back pain ; Low Back Pain - drug therapy ; Low Back Pain - genetics ; Low Back Pain - pathology ; Matrix Metalloproteinase 13 - genetics ; Matrix Metalloproteinase 3 - genetics ; Mitochondria ; NF-E2-Related Factor 2 - genetics ; Nrf2 ; Nuclei (cytology) ; Nucleus pulposus ; Nucleus Pulposus - drug effects ; Nucleus Pulposus - pathology ; Original ; p53 Protein ; Pain ; polydatin ; Rats ; Senescence ; Stilbenes - pharmacology ; Thrombospondin ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>Journal of cellular and molecular medicine, 2018-11, Vol.22 (11), p.5720-5731</ispartof><rights>2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2018. 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-c4488-c798dad6e5904287b2897933f7f5bfc2ed6276ecf0eeededcc69002398201da73</citedby><cites>FETCH-LOGICAL-c4488-c798dad6e5904287b2897933f7f5bfc2ed6276ecf0eeededcc69002398201da73</cites><orcidid>0000-0003-0117-7599 ; 0000-0003-3435-2277</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/PMC6201341/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6201341/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,1412,11543,27905,27906,45555,45556,46033,46457,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30358118$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Jianle</creatorcontrib><creatorcontrib>Huang, Chongan</creatorcontrib><creatorcontrib>Lin, Zongze</creatorcontrib><creatorcontrib>Pan, Xiangxiang</creatorcontrib><creatorcontrib>Chen, Jiaoxiang</creatorcontrib><creatorcontrib>Zheng, Gang</creatorcontrib><creatorcontrib>Tian, Naifeng</creatorcontrib><creatorcontrib>Yan, Yingzhao</creatorcontrib><creatorcontrib>Zhang, Zengjie</creatorcontrib><creatorcontrib>Hu, Jianing</creatorcontrib><creatorcontrib>Cheng, Pu</creatorcontrib><creatorcontrib>Wang, Xiangyang</creatorcontrib><creatorcontrib>Zhang, Xiaolei</creatorcontrib><title>Polydatin suppresses nucleus pulposus cell senescence, promotes matrix homeostasis and attenuates intervertebral disc degeneration in rats</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Intervertebral disc degeneration (IVDD) is one of the major causes of low back pain. Polydatin (PD) has been shown to exert multiple pharmacological effects on different diseases; here, we test the therapeutic potential of PD for IVDD. In in‐vitro experiments, we confirmed PD is nontoxic to nucleus pulposus cells (NPCs) under the concentration of 400 μmol/L. Furthermore, PD was able to decrease the level of senescence in TNF‐α‐treated NPCs, as indicated by β‐gal staining as well as senescence markers p53 and p16 expression. In the aspect of extracellular matrix (ECM), PD not only reduced metalloproteinase 3 (MMP‐3), metalloproteinase 13 (MMP‐13) and a disintegrin‐like and metalloproteinase thrombospondin type 1 motif 4 (ADAMTS‐4) expression, but also increased aggrecan and collagen II levels. Mitochondrion is closely related to cellular senescence and ECM homeostasis; mechanistically, we found PD may rescue TNF‐α‐induced mitochondrial dysfunction, and it may also promote Nrf2 expression and activity. Silencing Nrf2 partly abolished the protective effects of PD on mitochondrial homeostasis, senescence and ECM homeostasis in TNF‐α‐treated NPCs. Correspondingly, PD ameliorated IVDD in rat model by promoting Nrf2 activity, preserving ECM and inhibiting senescence in nucleus pulposus cells. To sum up, our study suggests that PD exerts protective effects in NPCs against IVDD and reveals the underlying mechanism of PD on Nrf2 activation in NPCs.</description><subject>ADAMTS4 Protein - genetics</subject><subject>Aggrecan</subject><subject>Aggrecans - genetics</subject><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Cellular Senescence - drug effects</subject><subject>Collagen (type II)</subject><subject>Collagen - genetics</subject><subject>Degeneration</subject><subject>Disease Models, Animal</subject><subject>Extracellular matrix</subject><subject>Extracellular Matrix - drug effects</subject><subject>Extracellular Matrix - genetics</subject><subject>Glucosides - pharmacology</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Intervertebral Disc - drug effects</subject><subject>Intervertebral Disc - pathology</subject><subject>intervertebral disc degeneration</subject><subject>Intervertebral Disc Degeneration - drug therapy</subject><subject>Intervertebral Disc Degeneration - genetics</subject><subject>Intervertebral Disc Degeneration - pathology</subject><subject>Intervertebral discs</subject><subject>Low back pain</subject><subject>Low Back Pain - drug therapy</subject><subject>Low Back Pain - genetics</subject><subject>Low Back Pain - pathology</subject><subject>Matrix Metalloproteinase 13 - genetics</subject><subject>Matrix Metalloproteinase 3 - genetics</subject><subject>Mitochondria</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>Nrf2</subject><subject>Nuclei (cytology)</subject><subject>Nucleus pulposus</subject><subject>Nucleus Pulposus - drug effects</subject><subject>Nucleus Pulposus - pathology</subject><subject>Original</subject><subject>p53 Protein</subject><subject>Pain</subject><subject>polydatin</subject><subject>Rats</subject><subject>Senescence</subject><subject>Stilbenes - pharmacology</subject><subject>Thrombospondin</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</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>eNp9kctuFDEQRVsIREJgwwcgS2xQxAQ_-mFvIqFRIKBEsIC15bGrE4-67cblTjK_wFfjYSYRsMAbl1RHx1W-VfWS0RNWzru1HccTJmQtH1WHrJF8UStRP97XTAp5UD1DXFMqWibU0-pAUNFIxuRh9fNrHDbOZB8IztOUABGQhNkOMCOZ5mGKWAoLw0AQAqCFYOEtmVIcYy7oaHLyd-Q6jhAxG_RITHDE5AxhNlvChwzpBlKGVTIDcR4tcXBVZKm8G0MBSKnwefWkNwPCi_19VH3_cPZteb64-PLx0_L9xcLWtZQL2ynpjGuhUbTmsltxqTolRN_1zaq3HFzLuxZsTwHAgbO2VZRyoSSnzJlOHFWnO-80r8bSh5DLXHpKfjRpo6Px-u9O8Nf6Kt7otghEzYrgzV6Q4o8ZMOux7FR-yASIM2rOeMNVJ2Rb0Nf_oOs4p1DW21J1qzraykId7yibImKC_mEYRvU2Yr2NWP-OuMCv_hz_Ab3PtABsB9z6ATb_UenPy8vLnfQXElO22w</recordid><startdate>201811</startdate><enddate>201811</enddate><creator>Wang, Jianle</creator><creator>Huang, Chongan</creator><creator>Lin, Zongze</creator><creator>Pan, Xiangxiang</creator><creator>Chen, Jiaoxiang</creator><creator>Zheng, Gang</creator><creator>Tian, Naifeng</creator><creator>Yan, Yingzhao</creator><creator>Zhang, Zengjie</creator><creator>Hu, Jianing</creator><creator>Cheng, Pu</creator><creator>Wang, Xiangyang</creator><creator>Zhang, Xiaolei</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/0000-0003-0117-7599</orcidid><orcidid>https://orcid.org/0000-0003-3435-2277</orcidid></search><sort><creationdate>201811</creationdate><title>Polydatin suppresses nucleus pulposus cell senescence, promotes matrix homeostasis and attenuates intervertebral disc degeneration in rats</title><author>Wang, Jianle ; Huang, Chongan ; Lin, Zongze ; Pan, Xiangxiang ; Chen, Jiaoxiang ; Zheng, Gang ; Tian, Naifeng ; Yan, Yingzhao ; Zhang, Zengjie ; Hu, Jianing ; Cheng, Pu ; Wang, Xiangyang ; Zhang, Xiaolei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4488-c798dad6e5904287b2897933f7f5bfc2ed6276ecf0eeededcc69002398201da73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>ADAMTS4 Protein - genetics</topic><topic>Aggrecan</topic><topic>Aggrecans - genetics</topic><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Cellular Senescence - drug effects</topic><topic>Collagen (type II)</topic><topic>Collagen - genetics</topic><topic>Degeneration</topic><topic>Disease Models, Animal</topic><topic>Extracellular matrix</topic><topic>Extracellular Matrix - drug effects</topic><topic>Extracellular Matrix - genetics</topic><topic>Glucosides - pharmacology</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Intervertebral Disc - drug effects</topic><topic>Intervertebral Disc - pathology</topic><topic>intervertebral disc degeneration</topic><topic>Intervertebral Disc Degeneration - drug therapy</topic><topic>Intervertebral Disc Degeneration - genetics</topic><topic>Intervertebral Disc Degeneration - pathology</topic><topic>Intervertebral discs</topic><topic>Low back pain</topic><topic>Low Back Pain - drug therapy</topic><topic>Low Back Pain - genetics</topic><topic>Low Back Pain - pathology</topic><topic>Matrix Metalloproteinase 13 - genetics</topic><topic>Matrix Metalloproteinase 3 - genetics</topic><topic>Mitochondria</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>Nrf2</topic><topic>Nuclei (cytology)</topic><topic>Nucleus pulposus</topic><topic>Nucleus Pulposus - drug effects</topic><topic>Nucleus Pulposus - pathology</topic><topic>Original</topic><topic>p53 Protein</topic><topic>Pain</topic><topic>polydatin</topic><topic>Rats</topic><topic>Senescence</topic><topic>Stilbenes - pharmacology</topic><topic>Thrombospondin</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Jianle</creatorcontrib><creatorcontrib>Huang, Chongan</creatorcontrib><creatorcontrib>Lin, Zongze</creatorcontrib><creatorcontrib>Pan, Xiangxiang</creatorcontrib><creatorcontrib>Chen, Jiaoxiang</creatorcontrib><creatorcontrib>Zheng, Gang</creatorcontrib><creatorcontrib>Tian, Naifeng</creatorcontrib><creatorcontrib>Yan, Yingzhao</creatorcontrib><creatorcontrib>Zhang, Zengjie</creatorcontrib><creatorcontrib>Hu, Jianing</creatorcontrib><creatorcontrib>Cheng, Pu</creatorcontrib><creatorcontrib>Wang, Xiangyang</creatorcontrib><creatorcontrib>Zhang, Xiaolei</creatorcontrib><collection>Wiley Online Library Open Access</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>Wang, Jianle</au><au>Huang, Chongan</au><au>Lin, Zongze</au><au>Pan, Xiangxiang</au><au>Chen, Jiaoxiang</au><au>Zheng, Gang</au><au>Tian, Naifeng</au><au>Yan, Yingzhao</au><au>Zhang, Zengjie</au><au>Hu, Jianing</au><au>Cheng, Pu</au><au>Wang, Xiangyang</au><au>Zhang, Xiaolei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polydatin suppresses nucleus pulposus cell senescence, promotes matrix homeostasis and attenuates intervertebral disc degeneration in rats</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2018-11</date><risdate>2018</risdate><volume>22</volume><issue>11</issue><spage>5720</spage><epage>5731</epage><pages>5720-5731</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Intervertebral disc degeneration (IVDD) is one of the major causes of low back pain. Polydatin (PD) has been shown to exert multiple pharmacological effects on different diseases; here, we test the therapeutic potential of PD for IVDD. In in‐vitro experiments, we confirmed PD is nontoxic to nucleus pulposus cells (NPCs) under the concentration of 400 μmol/L. Furthermore, PD was able to decrease the level of senescence in TNF‐α‐treated NPCs, as indicated by β‐gal staining as well as senescence markers p53 and p16 expression. In the aspect of extracellular matrix (ECM), PD not only reduced metalloproteinase 3 (MMP‐3), metalloproteinase 13 (MMP‐13) and a disintegrin‐like and metalloproteinase thrombospondin type 1 motif 4 (ADAMTS‐4) expression, but also increased aggrecan and collagen II levels. Mitochondrion is closely related to cellular senescence and ECM homeostasis; mechanistically, we found PD may rescue TNF‐α‐induced mitochondrial dysfunction, and it may also promote Nrf2 expression and activity. Silencing Nrf2 partly abolished the protective effects of PD on mitochondrial homeostasis, senescence and ECM homeostasis in TNF‐α‐treated NPCs. Correspondingly, PD ameliorated IVDD in rat model by promoting Nrf2 activity, preserving ECM and inhibiting senescence in nucleus pulposus cells. To sum up, our study suggests that PD exerts protective effects in NPCs against IVDD and reveals the underlying mechanism of PD on Nrf2 activation in NPCs.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>30358118</pmid><doi>10.1111/jcmm.13848</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-0117-7599</orcidid><orcidid>https://orcid.org/0000-0003-3435-2277</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cellular and molecular medicine, 2018-11, Vol.22 (11), p.5720-5731 |
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| language | eng |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Wiley Online Library Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | ADAMTS4 Protein - genetics Aggrecan Aggrecans - genetics Animals Cells, Cultured Cellular Senescence - drug effects Collagen (type II) Collagen - genetics Degeneration Disease Models, Animal Extracellular matrix Extracellular Matrix - drug effects Extracellular Matrix - genetics Glucosides - pharmacology Homeostasis Humans Intervertebral Disc - drug effects Intervertebral Disc - pathology intervertebral disc degeneration Intervertebral Disc Degeneration - drug therapy Intervertebral Disc Degeneration - genetics Intervertebral Disc Degeneration - pathology Intervertebral discs Low back pain Low Back Pain - drug therapy Low Back Pain - genetics Low Back Pain - pathology Matrix Metalloproteinase 13 - genetics Matrix Metalloproteinase 3 - genetics Mitochondria NF-E2-Related Factor 2 - genetics Nrf2 Nuclei (cytology) Nucleus pulposus Nucleus Pulposus - drug effects Nucleus Pulposus - pathology Original p53 Protein Pain polydatin Rats Senescence Stilbenes - pharmacology Thrombospondin Tumor Necrosis Factor-alpha - genetics |
| title | Polydatin suppresses nucleus pulposus cell senescence, promotes matrix homeostasis and attenuates intervertebral disc degeneration in rats |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T12%3A35%3A04IST&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=Polydatin%20suppresses%20nucleus%20pulposus%20cell%20senescence,%20promotes%20matrix%20homeostasis%20and%20attenuates%20intervertebral%20disc%20degeneration%20in%20rats&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Wang,%20Jianle&rft.date=2018-11&rft.volume=22&rft.issue=11&rft.spage=5720&rft.epage=5731&rft.pages=5720-5731&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.13848&rft_dat=%3Cproquest_pubme%3E2124697068%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=2124697068&rft_id=info:pmid/30358118&rfr_iscdi=true |