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
Hauptverfasser: Zhang, Xin, Hu, Can, Zhang, Ning, Wei, Wen-ying, Li, Ling-li, Wu, Hai-ming, Ma, Zhen-guo, Tang, Qi-zhu
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container_issue 4
container_start_page 573
container_title Acta pharmacologica Sinica
container_volume 42
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.
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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><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 &amp; 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 &amp; 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 ; 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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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