Matrine attenuates pathological cardiac fibrosis via RPS5/p38 in mice
Pathological cardiac fibrosis is a common feature in multiple cardiovascular diseases that contributes to the occurrence of heart failure and life-threatening arrhythmias. Our previous study demonstrated that matrine could attenuate doxorubicin-induced oxidative stress and cardiomyocyte apoptosis. I...
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Veröffentlicht in: | Acta pharmacologica Sinica 2021-04, Vol.42 (4), p.573-584 |
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creator | Zhang, Xin Hu, Can Zhang, Ning Wei, Wen-ying Li, Ling-li Wu, Hai-ming Ma, Zhen-guo Tang, Qi-zhu |
description | Pathological cardiac fibrosis is a common feature in multiple cardiovascular diseases that contributes to the occurrence of heart failure and life-threatening arrhythmias. Our previous study demonstrated that matrine could attenuate doxorubicin-induced oxidative stress and cardiomyocyte apoptosis. In this study, we investigated the effect of matrine on cardiac fibrosis. Mice received aortic banding (AB) operation or continuous injection of isoprenaline (ISO) to generate pathological cardiac fibrosis and then were exposed to matrine lavage (200 mg·kg
−1
·d
−1
) or an equal volume of vehicle as the control. We found that matrine lavage significantly attenuated AB or ISO-induced fibrotic remodeling and cardiac dysfunction. We also showed that matrine (200 μmol/L) significantly inhibited the proliferation, migration, collagen production, and phenotypic transdifferentiation of cardiac fibroblasts. Mechanistically, matrine suppressed p38 activation in vivo and in vitro, and overexpression of constitutively active p38 completely abolished the protective effects of matrine. We also demonstrated that ribosomal protein S5 (RPS5) upregulation was responsible for matrine-mediated inhibition on p38 and fibrogenesis. More importantly, matrine was capable of ameliorating preexisting cardiac fibrosis in mice. In conclusion, matrine treatment attenuates cardiac fibrosis by regulating RPS5/p38 signaling in mice, and it might be a promising therapeutic agent for treating pathological cardiac fibrosis. |
doi_str_mv | 10.1038/s41401-020-0473-8 |
format | Article |
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−1
·d
−1
) or an equal volume of vehicle as the control. We found that matrine lavage significantly attenuated AB or ISO-induced fibrotic remodeling and cardiac dysfunction. We also showed that matrine (200 μmol/L) significantly inhibited the proliferation, migration, collagen production, and phenotypic transdifferentiation of cardiac fibroblasts. Mechanistically, matrine suppressed p38 activation in vivo and in vitro, and overexpression of constitutively active p38 completely abolished the protective effects of matrine. We also demonstrated that ribosomal protein S5 (RPS5) upregulation was responsible for matrine-mediated inhibition on p38 and fibrogenesis. More importantly, matrine was capable of ameliorating preexisting cardiac fibrosis in mice. In conclusion, matrine treatment attenuates cardiac fibrosis by regulating RPS5/p38 signaling in mice, and it might be a promising therapeutic agent for treating pathological cardiac fibrosis.</description><identifier>ISSN: 1671-4083</identifier><identifier>EISSN: 1745-7254</identifier><identifier>DOI: 10.1038/s41401-020-0473-8</identifier><identifier>PMID: 32694761</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Alkaloids - therapeutic use ; Animals ; Aorta ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Biotechnology ; Cardiomyocytes ; Cardiomyopathies - chemically induced ; Cardiomyopathies - drug therapy ; Cardiotonic Agents - therapeutic use ; Cardiovascular diseases ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cell Transdifferentiation - drug effects ; Collagen ; Congestive heart failure ; Coronary vessels ; Doxorubicin ; Fibroblasts ; Fibroblasts - drug effects ; Fibrosis ; Fibrosis - chemically induced ; Fibrosis - drug therapy ; Growth factors ; Heart ; Heart - drug effects ; Immunology ; Internal Medicine ; Isoproterenol ; Kinases ; Laboratory animals ; Male ; MAP Kinase Signaling System - drug effects ; Matrines ; Medical Microbiology ; Mice ; Mice, Inbred C57BL ; Oxidative stress ; p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases - metabolism ; Pharmacology/Toxicology ; Proteins ; Quinolizines - therapeutic use ; Ribosomal protein S5 ; Ribosomal Proteins - metabolism ; Surgery ; Up-Regulation - drug effects ; Vaccine</subject><ispartof>Acta pharmacologica Sinica, 2021-04, Vol.42 (4), p.573-584</ispartof><rights>CPS and SIMM 2020</rights><rights>CPS and SIMM 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-a5085fa6239fdead3c5c0a7c2ab5ec11066b14e66c2e453d2184d538d30957853</citedby><cites>FETCH-LOGICAL-c470t-a5085fa6239fdead3c5c0a7c2ab5ec11066b14e66c2e453d2184d538d30957853</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/PMC8115053/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8115053/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32694761$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Xin</creatorcontrib><creatorcontrib>Hu, Can</creatorcontrib><creatorcontrib>Zhang, Ning</creatorcontrib><creatorcontrib>Wei, Wen-ying</creatorcontrib><creatorcontrib>Li, Ling-li</creatorcontrib><creatorcontrib>Wu, Hai-ming</creatorcontrib><creatorcontrib>Ma, Zhen-guo</creatorcontrib><creatorcontrib>Tang, Qi-zhu</creatorcontrib><title>Matrine attenuates pathological cardiac fibrosis via RPS5/p38 in mice</title><title>Acta pharmacologica Sinica</title><addtitle>Acta Pharmacol Sin</addtitle><addtitle>Acta Pharmacol Sin</addtitle><description>Pathological cardiac fibrosis is a common feature in multiple cardiovascular diseases that contributes to the occurrence of heart failure and life-threatening arrhythmias. Our previous study demonstrated that matrine could attenuate doxorubicin-induced oxidative stress and cardiomyocyte apoptosis. In this study, we investigated the effect of matrine on cardiac fibrosis. Mice received aortic banding (AB) operation or continuous injection of isoprenaline (ISO) to generate pathological cardiac fibrosis and then were exposed to matrine lavage (200 mg·kg
−1
·d
−1
) or an equal volume of vehicle as the control. We found that matrine lavage significantly attenuated AB or ISO-induced fibrotic remodeling and cardiac dysfunction. We also showed that matrine (200 μmol/L) significantly inhibited the proliferation, migration, collagen production, and phenotypic transdifferentiation of cardiac fibroblasts. Mechanistically, matrine suppressed p38 activation in vivo and in vitro, and overexpression of constitutively active p38 completely abolished the protective effects of matrine. We also demonstrated that ribosomal protein S5 (RPS5) upregulation was responsible for matrine-mediated inhibition on p38 and fibrogenesis. More importantly, matrine was capable of ameliorating preexisting cardiac fibrosis in mice. In conclusion, matrine treatment attenuates cardiac fibrosis by regulating RPS5/p38 signaling in mice, and it might be a promising therapeutic agent for treating pathological cardiac fibrosis.</description><subject>Alkaloids - therapeutic use</subject><subject>Animals</subject><subject>Aorta</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Biotechnology</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathies - chemically induced</subject><subject>Cardiomyopathies - drug therapy</subject><subject>Cardiotonic Agents - therapeutic use</subject><subject>Cardiovascular diseases</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Transdifferentiation - drug effects</subject><subject>Collagen</subject><subject>Congestive heart failure</subject><subject>Coronary vessels</subject><subject>Doxorubicin</subject><subject>Fibroblasts</subject><subject>Fibroblasts - drug effects</subject><subject>Fibrosis</subject><subject>Fibrosis - chemically induced</subject><subject>Fibrosis - drug therapy</subject><subject>Growth factors</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Immunology</subject><subject>Internal Medicine</subject><subject>Isoproterenol</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Matrines</subject><subject>Medical Microbiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Oxidative stress</subject><subject>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Pharmacology/Toxicology</subject><subject>Proteins</subject><subject>Quinolizines - therapeutic use</subject><subject>Ribosomal protein S5</subject><subject>Ribosomal Proteins - metabolism</subject><subject>Surgery</subject><subject>Up-Regulation - drug effects</subject><subject>Vaccine</subject><issn>1671-4083</issn><issn>1745-7254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><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>eNp1kU1r3DAQhkVoaNK0P6CXYuilFycajb58KZSQNoGElqQ9i1lZ3ih47a1kB_Lvo2XTfEFPEswzjzTzMvYR-CFwtEdZguRQc8FrLg3Wdoftg5GqNkLJN-WuDdSSW9xj73K-4RwFQvOW7aHQjTQa9tnJBU0pDqGiaQrDTFPI1Zqm67Efl9FTX3lKbSRfdXGRxhxzdRupuvx1pY7WaKs4VKvow3u221Gfw4eH84D9-X7y-_i0Pv_54-z423ntpeFTTYpb1ZEW2HRtoBa98pyMF7RQwQNwrRcgg9ZeBKmwFWBlq9C2yBtlrMID9nXrXc-LVWh9GKZEvVunuKJ050aK7mVliNduOd46C6C4wiL48iBI49855MmtYvah72kI45ydkEKDBdS2oJ9foTfjnIYynhOqrFwiNqZQsKV82U5OoXv8DHC3CcltQ3Klw21Cchvzp-dTPHb8S6UAYgvkUhqWIT09_X_rPSjrm54</recordid><startdate>20210401</startdate><enddate>20210401</enddate><creator>Zhang, Xin</creator><creator>Hu, Can</creator><creator>Zhang, Ning</creator><creator>Wei, Wen-ying</creator><creator>Li, Ling-li</creator><creator>Wu, Hai-ming</creator><creator>Ma, Zhen-guo</creator><creator>Tang, Qi-zhu</creator><general>Springer Singapore</general><general>Nature Publishing Group</general><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>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20210401</creationdate><title>Matrine attenuates pathological cardiac fibrosis via RPS5/p38 in mice</title><author>Zhang, Xin ; Hu, Can ; Zhang, Ning ; Wei, Wen-ying ; Li, Ling-li ; Wu, Hai-ming ; Ma, Zhen-guo ; Tang, Qi-zhu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-a5085fa6239fdead3c5c0a7c2ab5ec11066b14e66c2e453d2184d538d30957853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Alkaloids - therapeutic use</topic><topic>Animals</topic><topic>Aorta</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Biotechnology</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathies - chemically induced</topic><topic>Cardiomyopathies - drug therapy</topic><topic>Cardiotonic Agents - therapeutic use</topic><topic>Cardiovascular diseases</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Transdifferentiation - drug effects</topic><topic>Collagen</topic><topic>Congestive heart failure</topic><topic>Coronary vessels</topic><topic>Doxorubicin</topic><topic>Fibroblasts</topic><topic>Fibroblasts - drug effects</topic><topic>Fibrosis</topic><topic>Fibrosis - chemically induced</topic><topic>Fibrosis - drug therapy</topic><topic>Growth factors</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Immunology</topic><topic>Internal Medicine</topic><topic>Isoproterenol</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Matrines</topic><topic>Medical Microbiology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Oxidative stress</topic><topic>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Pharmacology/Toxicology</topic><topic>Proteins</topic><topic>Quinolizines - therapeutic use</topic><topic>Ribosomal protein S5</topic><topic>Ribosomal Proteins - metabolism</topic><topic>Surgery</topic><topic>Up-Regulation - drug effects</topic><topic>Vaccine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Xin</creatorcontrib><creatorcontrib>Hu, Can</creatorcontrib><creatorcontrib>Zhang, Ning</creatorcontrib><creatorcontrib>Wei, Wen-ying</creatorcontrib><creatorcontrib>Li, Ling-li</creatorcontrib><creatorcontrib>Wu, Hai-ming</creatorcontrib><creatorcontrib>Ma, Zhen-guo</creatorcontrib><creatorcontrib>Tang, Qi-zhu</creatorcontrib><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>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>AIDS and Cancer Research Abstracts</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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Acta pharmacologica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Xin</au><au>Hu, Can</au><au>Zhang, Ning</au><au>Wei, Wen-ying</au><au>Li, Ling-li</au><au>Wu, Hai-ming</au><au>Ma, Zhen-guo</au><au>Tang, Qi-zhu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Matrine attenuates pathological cardiac fibrosis via RPS5/p38 in mice</atitle><jtitle>Acta pharmacologica Sinica</jtitle><stitle>Acta Pharmacol Sin</stitle><addtitle>Acta Pharmacol Sin</addtitle><date>2021-04-01</date><risdate>2021</risdate><volume>42</volume><issue>4</issue><spage>573</spage><epage>584</epage><pages>573-584</pages><issn>1671-4083</issn><eissn>1745-7254</eissn><abstract>Pathological cardiac fibrosis is a common feature in multiple cardiovascular diseases that contributes to the occurrence of heart failure and life-threatening arrhythmias. Our previous study demonstrated that matrine could attenuate doxorubicin-induced oxidative stress and cardiomyocyte apoptosis. In this study, we investigated the effect of matrine on cardiac fibrosis. Mice received aortic banding (AB) operation or continuous injection of isoprenaline (ISO) to generate pathological cardiac fibrosis and then were exposed to matrine lavage (200 mg·kg
−1
·d
−1
) or an equal volume of vehicle as the control. We found that matrine lavage significantly attenuated AB or ISO-induced fibrotic remodeling and cardiac dysfunction. We also showed that matrine (200 μmol/L) significantly inhibited the proliferation, migration, collagen production, and phenotypic transdifferentiation of cardiac fibroblasts. Mechanistically, matrine suppressed p38 activation in vivo and in vitro, and overexpression of constitutively active p38 completely abolished the protective effects of matrine. We also demonstrated that ribosomal protein S5 (RPS5) upregulation was responsible for matrine-mediated inhibition on p38 and fibrogenesis. More importantly, matrine was capable of ameliorating preexisting cardiac fibrosis in mice. In conclusion, matrine treatment attenuates cardiac fibrosis by regulating RPS5/p38 signaling in mice, and it might be a promising therapeutic agent for treating pathological cardiac fibrosis.</abstract><cop>Singapore</cop><pub>Springer Singapore</pub><pmid>32694761</pmid><doi>10.1038/s41401-020-0473-8</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Alkaloids - therapeutic use Animals Aorta Apoptosis Biomedical and Life Sciences Biomedicine Biotechnology Cardiomyocytes Cardiomyopathies - chemically induced Cardiomyopathies - drug therapy Cardiotonic Agents - therapeutic use Cardiovascular diseases Cell Movement - drug effects Cell Proliferation - drug effects Cell Transdifferentiation - drug effects Collagen Congestive heart failure Coronary vessels Doxorubicin Fibroblasts Fibroblasts - drug effects Fibrosis Fibrosis - chemically induced Fibrosis - drug therapy Growth factors Heart Heart - drug effects Immunology Internal Medicine Isoproterenol Kinases Laboratory animals Male MAP Kinase Signaling System - drug effects Matrines Medical Microbiology Mice Mice, Inbred C57BL Oxidative stress p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - metabolism Pharmacology/Toxicology Proteins Quinolizines - therapeutic use Ribosomal protein S5 Ribosomal Proteins - metabolism Surgery Up-Regulation - drug effects Vaccine |
title | Matrine attenuates pathological cardiac fibrosis via RPS5/p38 in mice |
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