Novel liver fibrosis model in Macaca fascicularis induced by thioacetamide
Although transplantation is the only definitive treatment for liver cirrhosis, there remains a shortage of donors, necessitating that novel treatments be developed. We aimed to establish a liver fibrosis model in Macaca fascicularis that can help accelerate preclinical research. Liver fibrosis was i...
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| Veröffentlicht in: | Scientific reports 2020-02, Vol.10 (1), p.2450, Article 2450 |
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| creator | Matsuo, Megumi Murata, Soichiro Hasegawa, Shunsuke Hatada, Yumi Ohtsuka, Masayuki Taniguchi, Hideki |
| description | Although transplantation is the only definitive treatment for liver cirrhosis, there remains a shortage of donors, necessitating that novel treatments be developed. We aimed to establish a liver fibrosis model in
Macaca fascicularis
that can help accelerate preclinical research. Liver fibrosis was induced by administering thioacetamide (TAA) and carbon tetrachloride (CCl
4
). Analysis of residual liver function and fibrosis progression was based on clinical indices, such as the Child–Pugh score or fibrotic markers, besides histology. TAA-induced marked fibrosis, whereas CCl
4
did not induce fibrosis. Concerning residual liver function, both of TAA and CCl
4
worsened the indices of the Child–Pugh score, but only the TAA model increased the retention ratio of indocyanine green. The TAA-induced fibrosis model in
Macaca fascicularis
worsens fibrosis and residual liver function, mimicking Child–Pugh grade B. Given that our model was evaluated by clinical indices, it could be applicable to preclinical research. |
| doi_str_mv | 10.1038/s41598-020-58739-4 |
| format | Article |
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Macaca fascicularis
that can help accelerate preclinical research. Liver fibrosis was induced by administering thioacetamide (TAA) and carbon tetrachloride (CCl
4
). Analysis of residual liver function and fibrosis progression was based on clinical indices, such as the Child–Pugh score or fibrotic markers, besides histology. TAA-induced marked fibrosis, whereas CCl
4
did not induce fibrosis. Concerning residual liver function, both of TAA and CCl
4
worsened the indices of the Child–Pugh score, but only the TAA model increased the retention ratio of indocyanine green. The TAA-induced fibrosis model in
Macaca fascicularis
worsens fibrosis and residual liver function, mimicking Child–Pugh grade B. Given that our model was evaluated by clinical indices, it could be applicable to preclinical research.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-020-58739-4</identifier><identifier>PMID: 32051422</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 14/63 ; 692/4020/4021 ; 692/420/256 ; Animals ; Bile ; Carbon tetrachloride ; Cirrhosis ; Disease Models, Animal ; Disease Progression ; Fibrosis ; Histology ; Humanities and Social Sciences ; Liver ; Liver - drug effects ; Liver - pathology ; Liver - physiopathology ; Liver cirrhosis ; Liver Cirrhosis - chemically induced ; Liver Cirrhosis - pathology ; Liver Cirrhosis - physiopathology ; Liver Function Tests ; Macaca fascicularis ; Macaca fascicularis - physiology ; Mimicry ; multidisciplinary ; Science ; Science (multidisciplinary) ; Thioacetamide ; Transplantation</subject><ispartof>Scientific reports, 2020-02, Vol.10 (1), p.2450, Article 2450</ispartof><rights>The Author(s) 2020</rights><rights>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-c540t-3fbb6735bffb198b55d5f94747aea2a8e44f4368ba7b06de3ad7163ea56f4f1b3</citedby><cites>FETCH-LOGICAL-c540t-3fbb6735bffb198b55d5f94747aea2a8e44f4368ba7b06de3ad7163ea56f4f1b3</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/PMC7016167/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7016167/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32051422$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsuo, Megumi</creatorcontrib><creatorcontrib>Murata, Soichiro</creatorcontrib><creatorcontrib>Hasegawa, Shunsuke</creatorcontrib><creatorcontrib>Hatada, Yumi</creatorcontrib><creatorcontrib>Ohtsuka, Masayuki</creatorcontrib><creatorcontrib>Taniguchi, Hideki</creatorcontrib><title>Novel liver fibrosis model in Macaca fascicularis induced by thioacetamide</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Although transplantation is the only definitive treatment for liver cirrhosis, there remains a shortage of donors, necessitating that novel treatments be developed. We aimed to establish a liver fibrosis model in
Macaca fascicularis
that can help accelerate preclinical research. Liver fibrosis was induced by administering thioacetamide (TAA) and carbon tetrachloride (CCl
4
). Analysis of residual liver function and fibrosis progression was based on clinical indices, such as the Child–Pugh score or fibrotic markers, besides histology. TAA-induced marked fibrosis, whereas CCl
4
did not induce fibrosis. Concerning residual liver function, both of TAA and CCl
4
worsened the indices of the Child–Pugh score, but only the TAA model increased the retention ratio of indocyanine green. The TAA-induced fibrosis model in
Macaca fascicularis
worsens fibrosis and residual liver function, mimicking Child–Pugh grade B. Given that our model was evaluated by clinical indices, it could be applicable to preclinical research.</description><subject>13/51</subject><subject>14/63</subject><subject>692/4020/4021</subject><subject>692/420/256</subject><subject>Animals</subject><subject>Bile</subject><subject>Carbon tetrachloride</subject><subject>Cirrhosis</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Fibrosis</subject><subject>Histology</subject><subject>Humanities and Social Sciences</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - pathology</subject><subject>Liver - physiopathology</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis - chemically induced</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver Cirrhosis - physiopathology</subject><subject>Liver Function Tests</subject><subject>Macaca fascicularis</subject><subject>Macaca fascicularis - physiology</subject><subject>Mimicry</subject><subject>multidisciplinary</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Thioacetamide</subject><subject>Transplantation</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9UctOwzAQtBCIotIf4IAicQ74GScXJFTxVIELnC07sVtXSVzspFL_HkNKKRfsg1ee2ZnVDgBnCF4iSPKrQBEr8hRimLKckyKlB-AEQ8pSTDA-3KtHYBLCEsbDcEFRcQxGBEOGKMYn4OnFrXWd1HatfWKs8i7YkDSuip-2TZ5lGW9iZCht2dfSR9C2VV_qKlGbpFtYJ0vdycZW-hQcGVkHPdm-Y_B-d_s2fUhnr_eP05tZWjIKu5QYpTJOmDJGoSJXjFXMFJRTLrXEMteUGkqyXEmuYFZpIiuOMqIlyww1SJExuB50V71qdFXqtvOyFitvG-k3wkkr_iKtXYi5WwsOUYai9RhcbAW8--h16MTS9b6NMwtM4owF5wRGFh5YZdxJ8NrsHBAUXxGIIQIRIxDfEQgam873Z9u1_Cw8EshACBFq59r_ev8j-wmGR5L3</recordid><startdate>20200212</startdate><enddate>20200212</enddate><creator>Matsuo, Megumi</creator><creator>Murata, Soichiro</creator><creator>Hasegawa, Shunsuke</creator><creator>Hatada, Yumi</creator><creator>Ohtsuka, Masayuki</creator><creator>Taniguchi, Hideki</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>5PM</scope></search><sort><creationdate>20200212</creationdate><title>Novel liver fibrosis model in Macaca fascicularis induced by thioacetamide</title><author>Matsuo, Megumi ; Murata, Soichiro ; Hasegawa, Shunsuke ; Hatada, Yumi ; Ohtsuka, Masayuki ; Taniguchi, Hideki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-3fbb6735bffb198b55d5f94747aea2a8e44f4368ba7b06de3ad7163ea56f4f1b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>13/51</topic><topic>14/63</topic><topic>692/4020/4021</topic><topic>692/420/256</topic><topic>Animals</topic><topic>Bile</topic><topic>Carbon tetrachloride</topic><topic>Cirrhosis</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Fibrosis</topic><topic>Histology</topic><topic>Humanities and Social Sciences</topic><topic>Liver</topic><topic>Liver - drug effects</topic><topic>Liver - pathology</topic><topic>Liver - physiopathology</topic><topic>Liver cirrhosis</topic><topic>Liver Cirrhosis - chemically induced</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver Cirrhosis - physiopathology</topic><topic>Liver Function Tests</topic><topic>Macaca fascicularis</topic><topic>Macaca fascicularis - physiology</topic><topic>Mimicry</topic><topic>multidisciplinary</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Thioacetamide</topic><topic>Transplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsuo, Megumi</creatorcontrib><creatorcontrib>Murata, Soichiro</creatorcontrib><creatorcontrib>Hasegawa, Shunsuke</creatorcontrib><creatorcontrib>Hatada, Yumi</creatorcontrib><creatorcontrib>Ohtsuka, Masayuki</creatorcontrib><creatorcontrib>Taniguchi, Hideki</creatorcontrib><collection>Springer Nature OA Free Journals</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</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 One Sustainability</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>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>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 Basic</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>Matsuo, Megumi</au><au>Murata, Soichiro</au><au>Hasegawa, Shunsuke</au><au>Hatada, Yumi</au><au>Ohtsuka, Masayuki</au><au>Taniguchi, Hideki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Novel liver fibrosis model in Macaca fascicularis induced by thioacetamide</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2020-02-12</date><risdate>2020</risdate><volume>10</volume><issue>1</issue><spage>2450</spage><pages>2450-</pages><artnum>2450</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Although transplantation is the only definitive treatment for liver cirrhosis, there remains a shortage of donors, necessitating that novel treatments be developed. We aimed to establish a liver fibrosis model in
Macaca fascicularis
that can help accelerate preclinical research. Liver fibrosis was induced by administering thioacetamide (TAA) and carbon tetrachloride (CCl
4
). Analysis of residual liver function and fibrosis progression was based on clinical indices, such as the Child–Pugh score or fibrotic markers, besides histology. TAA-induced marked fibrosis, whereas CCl
4
did not induce fibrosis. Concerning residual liver function, both of TAA and CCl
4
worsened the indices of the Child–Pugh score, but only the TAA model increased the retention ratio of indocyanine green. The TAA-induced fibrosis model in
Macaca fascicularis
worsens fibrosis and residual liver function, mimicking Child–Pugh grade B. Given that our model was evaluated by clinical indices, it could be applicable to preclinical research.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32051422</pmid><doi>10.1038/s41598-020-58739-4</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 13/51 14/63 692/4020/4021 692/420/256 Animals Bile Carbon tetrachloride Cirrhosis Disease Models, Animal Disease Progression Fibrosis Histology Humanities and Social Sciences Liver Liver - drug effects Liver - pathology Liver - physiopathology Liver cirrhosis Liver Cirrhosis - chemically induced Liver Cirrhosis - pathology Liver Cirrhosis - physiopathology Liver Function Tests Macaca fascicularis Macaca fascicularis - physiology Mimicry multidisciplinary Science Science (multidisciplinary) Thioacetamide Transplantation |
| title | Novel liver fibrosis model in Macaca fascicularis induced by thioacetamide |
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