Emodin ameliorates bleomycin-induced pulmonary fibrosis in rats by suppressing epithelial-mesenchymal transition and fibroblast activation
Aberrant activation of TGF-β1 is frequently encountered and promotes epithelial-mesenchymal transition (EMT) and fibroblast activation in pulmonary fibrosis. The present study investigated whether emodin mediates its effect via suppressing TGF-β1-induced EMT and fibroblast activation in bleomycin (B...
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| description | Aberrant activation of TGF-β1 is frequently encountered and promotes epithelial-mesenchymal transition (EMT) and fibroblast activation in pulmonary fibrosis. The present study investigated whether emodin mediates its effect via suppressing TGF-β1-induced EMT and fibroblast activation in bleomycin (BLM)-induced pulmonary fibrosis in rats. Here, we found that emodin induced apoptosis and inhibited cellular proliferation, migration and differentiation in TGF-β1-stimulated human embryonic lung fibroblasts (HELFs). Emodin suppressed TGF-β1-induced EMT in a dose- and time-dependent manner in alveolar epithelial A549 cells. Emodin also inhibited TGF-β1-induced Smad2, Smad3 and Erk1/2 activation, suggesting that Smad2/3 and Erk1/2 inactivation mediated the emodin-induced effects on TGF-β1-induced EMT. Additionally, we provided
in vivo
evidence suggesting that emodin apparently alleviated BLM-induced pulmonary fibrosis and improved pulmonary function by inhibiting TGF-β1 signaling and subsequently repressing EMT, fibroblast activation and extracellular matrix (ECM) deposition. Taken together, our data suggest that emodin mediates its effects mainly via inhibition of EMT and fibroblast activation and thus has a potential for the treatment of pulmonary fibrosis. |
| doi_str_mv | 10.1038/srep35696 |
| format | Article |
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in vivo
evidence suggesting that emodin apparently alleviated BLM-induced pulmonary fibrosis and improved pulmonary function by inhibiting TGF-β1 signaling and subsequently repressing EMT, fibroblast activation and extracellular matrix (ECM) deposition. Taken together, our data suggest that emodin mediates its effects mainly via inhibition of EMT and fibroblast activation and thus has a potential for the treatment of pulmonary fibrosis.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep35696</identifier><identifier>PMID: 27774992</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 13/95 ; 14/19 ; 631/80/304 ; 692/699/1785 ; 82/80 ; 96/2 ; A549 Cells ; Alveolar Epithelial Cells - drug effects ; Alveolar Epithelial Cells - metabolism ; Alveoli ; Animals ; Apoptosis ; Bleomycin ; Bleomycin - pharmacology ; Cell Differentiation - drug effects ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Embryo fibroblasts ; Embryos ; Emodin ; Emodin - pharmacology ; Epithelial-Mesenchymal Transition - drug effects ; Extracellular matrix ; Extracellular Matrix - drug effects ; Extracellular Matrix - metabolism ; Fibroblasts ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Fibrosis ; Humanities and Social Sciences ; Humans ; Inactivation ; Lung - drug effects ; Lung - metabolism ; Lung diseases ; Male ; MAP Kinase Signaling System - drug effects ; Mesenchyme ; multidisciplinary ; Pulmonary fibrosis ; Pulmonary Fibrosis - chemically induced ; Pulmonary Fibrosis - drug therapy ; Pulmonary Fibrosis - metabolism ; Rats ; Rats, Sprague-Dawley ; Respiratory function ; Rodents ; Science ; Signal Transduction - drug effects ; Smad2 protein ; Smad2 Protein - metabolism ; Smad3 protein ; Smad3 Protein - metabolism ; Transforming Growth Factor beta1 - metabolism ; Transforming growth factor-b1</subject><ispartof>Scientific reports, 2016-10, Vol.6 (1), p.35696-35696, Article 35696</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Oct 2016</rights><rights>Copyright © 2016, The Author(s) 2016 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-ee50556e34746028e874173e9ed5518fc606d561993798d1ab27409cbb60f0443</citedby><cites>FETCH-LOGICAL-c438t-ee50556e34746028e874173e9ed5518fc606d561993798d1ab27409cbb60f0443</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/PMC5075925/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075925/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27922,27923,41118,42187,51574,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27774992$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guan, Ruijuan</creatorcontrib><creatorcontrib>Wang, Xia</creatorcontrib><creatorcontrib>Zhao, Xiaomei</creatorcontrib><creatorcontrib>Song, Nana</creatorcontrib><creatorcontrib>Zhu, Jimin</creatorcontrib><creatorcontrib>Wang, Jijiang</creatorcontrib><creatorcontrib>Wang, Jin</creatorcontrib><creatorcontrib>Xia, Chunmei</creatorcontrib><creatorcontrib>Chen, Yonghua</creatorcontrib><creatorcontrib>Zhu, Danian</creatorcontrib><creatorcontrib>Shen, Linlin</creatorcontrib><title>Emodin ameliorates bleomycin-induced pulmonary fibrosis in rats by suppressing epithelial-mesenchymal transition and fibroblast activation</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Aberrant activation of TGF-β1 is frequently encountered and promotes epithelial-mesenchymal transition (EMT) and fibroblast activation in pulmonary fibrosis. The present study investigated whether emodin mediates its effect via suppressing TGF-β1-induced EMT and fibroblast activation in bleomycin (BLM)-induced pulmonary fibrosis in rats. Here, we found that emodin induced apoptosis and inhibited cellular proliferation, migration and differentiation in TGF-β1-stimulated human embryonic lung fibroblasts (HELFs). Emodin suppressed TGF-β1-induced EMT in a dose- and time-dependent manner in alveolar epithelial A549 cells. Emodin also inhibited TGF-β1-induced Smad2, Smad3 and Erk1/2 activation, suggesting that Smad2/3 and Erk1/2 inactivation mediated the emodin-induced effects on TGF-β1-induced EMT. Additionally, we provided
in vivo
evidence suggesting that emodin apparently alleviated BLM-induced pulmonary fibrosis and improved pulmonary function by inhibiting TGF-β1 signaling and subsequently repressing EMT, fibroblast activation and extracellular matrix (ECM) deposition. Taken together, our data suggest that emodin mediates its effects mainly via inhibition of EMT and fibroblast activation and thus has a potential for the treatment of pulmonary fibrosis.</description><subject>13/51</subject><subject>13/95</subject><subject>14/19</subject><subject>631/80/304</subject><subject>692/699/1785</subject><subject>82/80</subject><subject>96/2</subject><subject>A549 Cells</subject><subject>Alveolar Epithelial Cells - drug effects</subject><subject>Alveolar Epithelial Cells - metabolism</subject><subject>Alveoli</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Bleomycin</subject><subject>Bleomycin - pharmacology</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Embryo fibroblasts</subject><subject>Embryos</subject><subject>Emodin</subject><subject>Emodin - pharmacology</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Extracellular matrix</subject><subject>Extracellular Matrix - drug effects</subject><subject>Extracellular Matrix - metabolism</subject><subject>Fibroblasts</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>Fibrosis</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Inactivation</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>Lung diseases</subject><subject>Male</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Mesenchyme</subject><subject>multidisciplinary</subject><subject>Pulmonary fibrosis</subject><subject>Pulmonary Fibrosis - chemically induced</subject><subject>Pulmonary Fibrosis - drug therapy</subject><subject>Pulmonary Fibrosis - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Respiratory function</subject><subject>Rodents</subject><subject>Science</subject><subject>Signal Transduction - drug effects</subject><subject>Smad2 protein</subject><subject>Smad2 Protein - metabolism</subject><subject>Smad3 protein</subject><subject>Smad3 Protein - metabolism</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Transforming growth factor-b1</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</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>eNplkcFq3DAQhk1paUKaQ1-gGHppC04lWbKkSyGEtA0EcknPQpbHuwqy5Ep2YF-hT90Jmy7bVhcJ5tM__8xfVW8puaCkVZ9LhrkVne5eVKeMcNGwlrGXR--T6ryUB4JHMM2pfl2dMCkl15qdVr-upzT4WNsJgk_ZLlDqPkCads7HxsdhdTDU8xqmFG3e1aPvcyq-1PgHaYR3dVnnOUMpPm5qmP2yRSkbmgkKRLfdTTbUS7ax-MUn7BSHvUofbFlq6xb_aJ8qb6pXow0Fzp_vs-rH1-v7q-_N7d23m6vL28bxVi0NgCBCdNByyTvCFCjJqWxBwyAEVaPrSDeIjmrdSq0GansmOdGu7zsyEs7bs-rLXnde-wkGBxHdBTNnP-GEJllv_q5EvzWb9GgEkUIzgQIfngVy-rlCWczki4MQbIS0FkNVi04I0xLR9_-gD2nNEcdDSmvKiFIKqY97yuFuMc_xYIYS8xSyOYSM7Ltj9wfyT6QIfNoDBUtxA_mo5X9qvwGZ1bSI</recordid><startdate>20161024</startdate><enddate>20161024</enddate><creator>Guan, Ruijuan</creator><creator>Wang, Xia</creator><creator>Zhao, Xiaomei</creator><creator>Song, Nana</creator><creator>Zhu, Jimin</creator><creator>Wang, Jijiang</creator><creator>Wang, Jin</creator><creator>Xia, Chunmei</creator><creator>Chen, Yonghua</creator><creator>Zhu, Danian</creator><creator>Shen, Linlin</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</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>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161024</creationdate><title>Emodin ameliorates bleomycin-induced pulmonary fibrosis in rats by suppressing epithelial-mesenchymal transition and fibroblast activation</title><author>Guan, Ruijuan ; Wang, Xia ; Zhao, Xiaomei ; Song, Nana ; Zhu, Jimin ; Wang, Jijiang ; Wang, Jin ; Xia, Chunmei ; Chen, Yonghua ; Zhu, Danian ; Shen, Linlin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-ee50556e34746028e874173e9ed5518fc606d561993798d1ab27409cbb60f0443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>13/51</topic><topic>13/95</topic><topic>14/19</topic><topic>631/80/304</topic><topic>692/699/1785</topic><topic>82/80</topic><topic>96/2</topic><topic>A549 Cells</topic><topic>Alveolar Epithelial Cells - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guan, Ruijuan</au><au>Wang, Xia</au><au>Zhao, Xiaomei</au><au>Song, Nana</au><au>Zhu, Jimin</au><au>Wang, Jijiang</au><au>Wang, Jin</au><au>Xia, Chunmei</au><au>Chen, Yonghua</au><au>Zhu, Danian</au><au>Shen, Linlin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Emodin ameliorates bleomycin-induced pulmonary fibrosis in rats by suppressing epithelial-mesenchymal transition and fibroblast activation</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2016-10-24</date><risdate>2016</risdate><volume>6</volume><issue>1</issue><spage>35696</spage><epage>35696</epage><pages>35696-35696</pages><artnum>35696</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Aberrant activation of TGF-β1 is frequently encountered and promotes epithelial-mesenchymal transition (EMT) and fibroblast activation in pulmonary fibrosis. The present study investigated whether emodin mediates its effect via suppressing TGF-β1-induced EMT and fibroblast activation in bleomycin (BLM)-induced pulmonary fibrosis in rats. Here, we found that emodin induced apoptosis and inhibited cellular proliferation, migration and differentiation in TGF-β1-stimulated human embryonic lung fibroblasts (HELFs). Emodin suppressed TGF-β1-induced EMT in a dose- and time-dependent manner in alveolar epithelial A549 cells. Emodin also inhibited TGF-β1-induced Smad2, Smad3 and Erk1/2 activation, suggesting that Smad2/3 and Erk1/2 inactivation mediated the emodin-induced effects on TGF-β1-induced EMT. Additionally, we provided
in vivo
evidence suggesting that emodin apparently alleviated BLM-induced pulmonary fibrosis and improved pulmonary function by inhibiting TGF-β1 signaling and subsequently repressing EMT, fibroblast activation and extracellular matrix (ECM) deposition. Taken together, our data suggest that emodin mediates its effects mainly via inhibition of EMT and fibroblast activation and thus has a potential for the treatment of pulmonary fibrosis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27774992</pmid><doi>10.1038/srep35696</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/51 13/95 14/19 631/80/304 692/699/1785 82/80 96/2 A549 Cells Alveolar Epithelial Cells - drug effects Alveolar Epithelial Cells - metabolism Alveoli Animals Apoptosis Bleomycin Bleomycin - pharmacology Cell Differentiation - drug effects Cell Line, Tumor Cell Proliferation - drug effects Embryo fibroblasts Embryos Emodin Emodin - pharmacology Epithelial-Mesenchymal Transition - drug effects Extracellular matrix Extracellular Matrix - drug effects Extracellular Matrix - metabolism Fibroblasts Fibroblasts - drug effects Fibroblasts - metabolism Fibrosis Humanities and Social Sciences Humans Inactivation Lung - drug effects Lung - metabolism Lung diseases Male MAP Kinase Signaling System - drug effects Mesenchyme multidisciplinary Pulmonary fibrosis Pulmonary Fibrosis - chemically induced Pulmonary Fibrosis - drug therapy Pulmonary Fibrosis - metabolism Rats Rats, Sprague-Dawley Respiratory function Rodents Science Signal Transduction - drug effects Smad2 protein Smad2 Protein - metabolism Smad3 protein Smad3 Protein - metabolism Transforming Growth Factor beta1 - metabolism Transforming growth factor-b1 |
| title | Emodin ameliorates bleomycin-induced pulmonary fibrosis in rats by suppressing epithelial-mesenchymal transition and fibroblast activation |
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