Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-[beta]1/Smad2-Mediated Endothelial-to-Mesenchymal Transition
Background. Puerarin is a kind of flavonoids and is extracted from Chinese herb Kudzu root. Puerarin is widely used as an adjuvant therapy in Chinese clinics. But little is known about its effects on regulating cardiac fibrosis. Methods. Mice were subjected to transverse aorta constriction (TAC) for...
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| description | Background. Puerarin is a kind of flavonoids and is extracted from Chinese herb Kudzu root. Puerarin is widely used as an adjuvant therapy in Chinese clinics. But little is known about its effects on regulating cardiac fibrosis. Methods. Mice were subjected to transverse aorta constriction (TAC) for 8 weeks; meanwhile puerarin was given 1 week after TAC. Cardiac fibrosis was assessed by pathological staining. The mRNA and protein changes of CD31 and vimentin in both animal and human umbilical vein endothelial cells (HUVECs) models were detected. Immunofluorescence colocalization of CD31 and vimentin and scratch test were carried out to examine TGF-[beta]1-induced changes in HUVECs. The agonist and antagonist of peroxisome proliferator-activated receptor-[gamma] (PPAR-[gamma]) were used to explore the underlying mechanism. Results. Puerarin mitigated TAC-induced cardiac fibrosis, accompanied with suppressed endothelial-to-mesenchymal transition (EndMT). The consistent results were achieved in HUVECs model. TGF-[beta]1/Smad2 signaling pathway was blunted and PPAR-[gamma] expression was upregulated in puerarin-treated mice and HUVECs. Pioglitazone could reproduce the protective effect in HUVECs, while GW9662 reversed this effect imposed by puerarin. Conclusion. Puerarin protected against TAC-induced cardiac fibrosis, and this protective effect may be attributed to the upregulation of PPAR-[gamma] and the inhibition of TGF-[beta]1/Smad2-mediated EndMT. |
| doi_str_mv | 10.1155/2017/2647129 |
| format | Article |
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Puerarin is a kind of flavonoids and is extracted from Chinese herb Kudzu root. Puerarin is widely used as an adjuvant therapy in Chinese clinics. But little is known about its effects on regulating cardiac fibrosis. Methods. Mice were subjected to transverse aorta constriction (TAC) for 8 weeks; meanwhile puerarin was given 1 week after TAC. Cardiac fibrosis was assessed by pathological staining. The mRNA and protein changes of CD31 and vimentin in both animal and human umbilical vein endothelial cells (HUVECs) models were detected. Immunofluorescence colocalization of CD31 and vimentin and scratch test were carried out to examine TGF-[beta]1-induced changes in HUVECs. The agonist and antagonist of peroxisome proliferator-activated receptor-[gamma] (PPAR-[gamma]) were used to explore the underlying mechanism. Results. Puerarin mitigated TAC-induced cardiac fibrosis, accompanied with suppressed endothelial-to-mesenchymal transition (EndMT). The consistent results were achieved in HUVECs model. TGF-[beta]1/Smad2 signaling pathway was blunted and PPAR-[gamma] expression was upregulated in puerarin-treated mice and HUVECs. Pioglitazone could reproduce the protective effect in HUVECs, while GW9662 reversed this effect imposed by puerarin. Conclusion. Puerarin protected against TAC-induced cardiac fibrosis, and this protective effect may be attributed to the upregulation of PPAR-[gamma] and the inhibition of TGF-[beta]1/Smad2-mediated EndMT.</description><identifier>ISSN: 1687-4757</identifier><identifier>EISSN: 1687-4765</identifier><identifier>DOI: 10.1155/2017/2647129</identifier><language>eng</language><publisher>New York: John Wiley & Sons, Inc</publisher><subject>Angina pectoris ; Cardiology ; Cardiomyopathy ; Collagen ; Diabetes ; Fibroblasts ; Fibrosis ; Health aspects ; Heart ; Heart diseases ; Isoflavones ; Kinases ; Kudzu ; Laboratory animals ; Medicinal plants ; Phosphorylation ; Physiological aspects ; Prevention ; Proteins ; Studies ; Transforming growth factors</subject><ispartof>PPAR research, 2017-01, Vol.2017</ispartof><rights>COPYRIGHT 2017 John Wiley & Sons, Inc.</rights><rights>Copyright © 2017 Ya-Ge Jin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,27923,27924</link.rule.ids></links><search><creatorcontrib>Jin, Ya-Ge</creatorcontrib><creatorcontrib>Yuan, Yuan</creatorcontrib><creatorcontrib>Wu, Qing-Qing</creatorcontrib><creatorcontrib>Zhang, Ning</creatorcontrib><creatorcontrib>Fan, Di</creatorcontrib><creatorcontrib>Che, Yan</creatorcontrib><creatorcontrib>Wang, Zhao- Peng</creatorcontrib><creatorcontrib>Xiao, Yang</creatorcontrib><creatorcontrib>Wang, Sha-Sha</creatorcontrib><creatorcontrib>Tang, Qi-Zhu</creatorcontrib><title>Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-[beta]1/Smad2-Mediated Endothelial-to-Mesenchymal Transition</title><title>PPAR research</title><description>Background. Puerarin is a kind of flavonoids and is extracted from Chinese herb Kudzu root. Puerarin is widely used as an adjuvant therapy in Chinese clinics. But little is known about its effects on regulating cardiac fibrosis. Methods. Mice were subjected to transverse aorta constriction (TAC) for 8 weeks; meanwhile puerarin was given 1 week after TAC. Cardiac fibrosis was assessed by pathological staining. The mRNA and protein changes of CD31 and vimentin in both animal and human umbilical vein endothelial cells (HUVECs) models were detected. Immunofluorescence colocalization of CD31 and vimentin and scratch test were carried out to examine TGF-[beta]1-induced changes in HUVECs. The agonist and antagonist of peroxisome proliferator-activated receptor-[gamma] (PPAR-[gamma]) were used to explore the underlying mechanism. Results. Puerarin mitigated TAC-induced cardiac fibrosis, accompanied with suppressed endothelial-to-mesenchymal transition (EndMT). The consistent results were achieved in HUVECs model. TGF-[beta]1/Smad2 signaling pathway was blunted and PPAR-[gamma] expression was upregulated in puerarin-treated mice and HUVECs. Pioglitazone could reproduce the protective effect in HUVECs, while GW9662 reversed this effect imposed by puerarin. Conclusion. Puerarin protected against TAC-induced cardiac fibrosis, and this protective effect may be attributed to the upregulation of PPAR-[gamma] and the inhibition of TGF-[beta]1/Smad2-mediated EndMT.</description><subject>Angina pectoris</subject><subject>Cardiology</subject><subject>Cardiomyopathy</subject><subject>Collagen</subject><subject>Diabetes</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Health aspects</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Isoflavones</subject><subject>Kinases</subject><subject>Kudzu</subject><subject>Laboratory animals</subject><subject>Medicinal plants</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Prevention</subject><subject>Proteins</subject><subject>Studies</subject><subject>Transforming growth factors</subject><issn>1687-4757</issn><issn>1687-4765</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkFFLwzAUhYMoOKdv_oCAz3XJbdM0j2NsczBxYN9ESpqma0aXaJIh_gj_s8WJ-iD34V4O3zkHLkLXlNxSytgECOUTyDNOQZygEc0LnmQ8Z6c_N-Pn6CKEHSEsTYGM0MfmoL30xuKNd1GrGLDcSmNDxDPpGyMVXpjau2ACnobglJFRN_jNxA7HTuOV7UxtonEWuxaXy0XyVOson-nkcS8bSO51c3TMbeMGQ29kn0Q36EFb1b3vZY9LL234yrhEZ63sg7763mNULubl7C5ZPyxXs-k62QqWJgw4KaRoGs4Ey6AusgygBqqEVBwgL1pONActNCtYW9fQ6gIyQds0zbmqRTpGN8fYF-9eDzrEaucO3g6NFRWkSCGjIv2ltrLXlbGti16qvQmqmrIsH94sgA3U7T_UMI3eG-Wsbs2g_zF8ArHKgJU</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Jin, Ya-Ge</creator><creator>Yuan, Yuan</creator><creator>Wu, Qing-Qing</creator><creator>Zhang, Ning</creator><creator>Fan, Di</creator><creator>Che, Yan</creator><creator>Wang, Zhao- Peng</creator><creator>Xiao, Yang</creator><creator>Wang, Sha-Sha</creator><creator>Tang, Qi-Zhu</creator><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</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>CWDGH</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>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20170101</creationdate><title>Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-[beta]1/Smad2-Mediated Endothelial-to-Mesenchymal Transition</title><author>Jin, Ya-Ge ; Yuan, Yuan ; Wu, Qing-Qing ; Zhang, Ning ; Fan, Di ; Che, Yan ; Wang, Zhao- Peng ; Xiao, Yang ; Wang, Sha-Sha ; Tang, Qi-Zhu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g953-52708a9dd759542b84422b21c9ac72268f70e72e9e585fbb2fe82491f3367cb93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Angina pectoris</topic><topic>Cardiology</topic><topic>Cardiomyopathy</topic><topic>Collagen</topic><topic>Diabetes</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Health aspects</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Isoflavones</topic><topic>Kinases</topic><topic>Kudzu</topic><topic>Laboratory animals</topic><topic>Medicinal plants</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Prevention</topic><topic>Proteins</topic><topic>Studies</topic><topic>Transforming growth factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jin, Ya-Ge</creatorcontrib><creatorcontrib>Yuan, Yuan</creatorcontrib><creatorcontrib>Wu, Qing-Qing</creatorcontrib><creatorcontrib>Zhang, Ning</creatorcontrib><creatorcontrib>Fan, Di</creatorcontrib><creatorcontrib>Che, Yan</creatorcontrib><creatorcontrib>Wang, Zhao- Peng</creatorcontrib><creatorcontrib>Xiao, Yang</creatorcontrib><creatorcontrib>Wang, Sha-Sha</creatorcontrib><creatorcontrib>Tang, Qi-Zhu</creatorcontrib><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest Pharma Collection</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>Middle East & Africa Database</collection><collection>ProQuest Central Korea</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>Biological Science Database</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><jtitle>PPAR research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jin, Ya-Ge</au><au>Yuan, Yuan</au><au>Wu, Qing-Qing</au><au>Zhang, Ning</au><au>Fan, Di</au><au>Che, Yan</au><au>Wang, Zhao- Peng</au><au>Xiao, Yang</au><au>Wang, Sha-Sha</au><au>Tang, Qi-Zhu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-[beta]1/Smad2-Mediated Endothelial-to-Mesenchymal Transition</atitle><jtitle>PPAR research</jtitle><date>2017-01-01</date><risdate>2017</risdate><volume>2017</volume><issn>1687-4757</issn><eissn>1687-4765</eissn><abstract>Background. Puerarin is a kind of flavonoids and is extracted from Chinese herb Kudzu root. Puerarin is widely used as an adjuvant therapy in Chinese clinics. But little is known about its effects on regulating cardiac fibrosis. Methods. Mice were subjected to transverse aorta constriction (TAC) for 8 weeks; meanwhile puerarin was given 1 week after TAC. Cardiac fibrosis was assessed by pathological staining. The mRNA and protein changes of CD31 and vimentin in both animal and human umbilical vein endothelial cells (HUVECs) models were detected. Immunofluorescence colocalization of CD31 and vimentin and scratch test were carried out to examine TGF-[beta]1-induced changes in HUVECs. The agonist and antagonist of peroxisome proliferator-activated receptor-[gamma] (PPAR-[gamma]) were used to explore the underlying mechanism. Results. Puerarin mitigated TAC-induced cardiac fibrosis, accompanied with suppressed endothelial-to-mesenchymal transition (EndMT). The consistent results were achieved in HUVECs model. TGF-[beta]1/Smad2 signaling pathway was blunted and PPAR-[gamma] expression was upregulated in puerarin-treated mice and HUVECs. Pioglitazone could reproduce the protective effect in HUVECs, while GW9662 reversed this effect imposed by puerarin. Conclusion. Puerarin protected against TAC-induced cardiac fibrosis, and this protective effect may be attributed to the upregulation of PPAR-[gamma] and the inhibition of TGF-[beta]1/Smad2-mediated EndMT.</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><doi>10.1155/2017/2647129</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Angina pectoris Cardiology Cardiomyopathy Collagen Diabetes Fibroblasts Fibrosis Health aspects Heart Heart diseases Isoflavones Kinases Kudzu Laboratory animals Medicinal plants Phosphorylation Physiological aspects Prevention Proteins Studies Transforming growth factors |
| title | Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-[beta]1/Smad2-Mediated Endothelial-to-Mesenchymal Transition |
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