Locostatin Alleviates Liver Fibrosis Induced by Carbon Tetrachloride in Mice
Background and Aims Liver fibrosis is featured with excessive deposition of extracellular matrix and fibrous connective tissue hyperplasia. The specific inhibitor of Raf-1 kinase inhibitor protein, locostatin, inhibits the migration of hepatic stellate cells. In this study, we investigated the effec...
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| Veröffentlicht in: | Digestive diseases and sciences 2019-09, Vol.64 (9), p.2570-2580 |
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| creator | Ma, Junji Qiu, Yuzi Wang, Min Zhang, Ming Zhao, Xiaoyi Jiang, Huiqing |
| description | Background and Aims
Liver fibrosis is featured with excessive deposition of extracellular matrix and fibrous connective tissue hyperplasia. The specific inhibitor of Raf-1 kinase inhibitor protein, locostatin, inhibits the migration of hepatic stellate cells. In this study, we investigated the effect of locostatin on liver fibrosis and its underlying mechanism.
Methods
Carbon tetrachloride (CCl4) was used to induce liver fibrosis in mice, and locostatin was injected intraperitoneally. Liver fibrosis was assessed by Masson and Sirius red staining, hydroxyproline (HYP) assay, and collagen percentage area. Collagen I, collagen III, and α-SMA were detected by RT-PCR and western blot. The levels of MMP-13, MMP-2, TIMP-1, and TIMP-2 were estimated by ELISA. Liver inflammation was evaluated by HE staining and immunohistochemistry; liver myeloperoxidase (MPO), superoxide dismutase, and malondialdehyde were measured by ELISA; and cytokines were by Mouse Cytokine Array Q4000.
Results
Compared to the CCl4 group, HYP (208.56 ± 6.12) µg/g, percentage of total collagen at overall region (1.91 ± 0.13), MMP-13/TIMP-1 (0.19 ± 0.01), MPO (1.45 ± 0.04) U/g, TGF-β (2652 ± 91.20), PDGF-AA (3897 ± 290.69), and E-selectin (1569 ± 66.48) in the liver tissues were decreased significantly in the locostatin-treated group.
Conclusions
Locostatin mitigated liver fibrosis and inflammation induced by CCl4. The mechanism is via inhibition inflammatory cytokines, TGF-β, PDGF-AA, and E-selectin. |
| doi_str_mv | 10.1007/s10620-019-05588-5 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2193168187</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A712936395</galeid><sourcerecordid>A712936395</sourcerecordid><originalsourceid>FETCH-LOGICAL-c442t-ec65086c07ee37ac47c0a089dfde54a512551c6aaf4518ae0ec93999c1c9f8423</originalsourceid><addsrcrecordid>eNp9kU9v1DAQxS0EotvCF-CAInHhkjITx_-OqxWFSkFcytnyOpPiKhsXO6nUb4_DllYghHywNf69p5l5jL1BOEcA9SEjyAZqQFODEFrX4hnboFC8boTUz9kGUJY3ojxhpznfAIBRKF-yEw5atUabDeu66GOe3RymajuOdBfcTLnqwh2l6iLsU8whV5dTv3jqq_19tXNpH6fqiubk_PcxptBTVcRfgqdX7MXgxkyvH-4z9u3i49Xuc919_XS523a1b9tmrslLAVp6UERcOd8qDw606YeeROsENkKgl84NrUDtCMgbbozx6M2g24afsfdH39sUfyyUZ3sI2dM4uonikm2DhqPUqFVB3_2F3sQlTaW7lcKGC6ngibp2I9kwDXGdbjW1W4WN4ZIbUajzf1Dl9HQIPk40hFL_Q9AcBb6sMSca7G0KB5fuLYJdI7THCG2J0P6K0K6itw8dL_sD9Y-S35kVgB-BXL6ma0pPI_3H9ic54qPo</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2191235670</pqid></control><display><type>article</type><title>Locostatin Alleviates Liver Fibrosis Induced by Carbon Tetrachloride in Mice</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Ma, Junji ; Qiu, Yuzi ; Wang, Min ; Zhang, Ming ; Zhao, Xiaoyi ; Jiang, Huiqing</creator><creatorcontrib>Ma, Junji ; Qiu, Yuzi ; Wang, Min ; Zhang, Ming ; Zhao, Xiaoyi ; Jiang, Huiqing</creatorcontrib><description>Background and Aims
Liver fibrosis is featured with excessive deposition of extracellular matrix and fibrous connective tissue hyperplasia. The specific inhibitor of Raf-1 kinase inhibitor protein, locostatin, inhibits the migration of hepatic stellate cells. In this study, we investigated the effect of locostatin on liver fibrosis and its underlying mechanism.
Methods
Carbon tetrachloride (CCl4) was used to induce liver fibrosis in mice, and locostatin was injected intraperitoneally. Liver fibrosis was assessed by Masson and Sirius red staining, hydroxyproline (HYP) assay, and collagen percentage area. Collagen I, collagen III, and α-SMA were detected by RT-PCR and western blot. The levels of MMP-13, MMP-2, TIMP-1, and TIMP-2 were estimated by ELISA. Liver inflammation was evaluated by HE staining and immunohistochemistry; liver myeloperoxidase (MPO), superoxide dismutase, and malondialdehyde were measured by ELISA; and cytokines were by Mouse Cytokine Array Q4000.
Results
Compared to the CCl4 group, HYP (208.56 ± 6.12) µg/g, percentage of total collagen at overall region (1.91 ± 0.13), MMP-13/TIMP-1 (0.19 ± 0.01), MPO (1.45 ± 0.04) U/g, TGF-β (2652 ± 91.20), PDGF-AA (3897 ± 290.69), and E-selectin (1569 ± 66.48) in the liver tissues were decreased significantly in the locostatin-treated group.
Conclusions
Locostatin mitigated liver fibrosis and inflammation induced by CCl4. The mechanism is via inhibition inflammatory cytokines, TGF-β, PDGF-AA, and E-selectin.</description><identifier>ISSN: 0163-2116</identifier><identifier>EISSN: 1573-2568</identifier><identifier>DOI: 10.1007/s10620-019-05588-5</identifier><identifier>PMID: 30874989</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Actins - genetics ; Actins - metabolism ; Animals ; Bile ; Biochemistry ; Carbon Tetrachloride ; Cell Movement - drug effects ; Collagen ; Collagen Type I - genetics ; Collagen Type I - metabolism ; Collagen Type II - genetics ; Collagen Type II - metabolism ; Cytokines ; E-Selectin - metabolism ; Enzyme-linked immunosorbent assay ; Fibrosis ; Gastroenterology ; Hepatic Stellate Cells - physiology ; Hepatology ; Hydroxyproline - metabolism ; Hyperplasia ; Liver ; Liver Cirrhosis - chemically induced ; Liver Cirrhosis - drug therapy ; Liver Cirrhosis - metabolism ; Liver Cirrhosis - pathology ; Liver diseases ; Male ; Matrix Metalloproteinase 13 - genetics ; Matrix Metalloproteinase 13 - metabolism ; Matrix Metalloproteinase 2 - genetics ; Matrix Metalloproteinase 2 - metabolism ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred C57BL ; Oncology ; Original Article ; Oxazolidinones - pharmacology ; Oxazolidinones - therapeutic use ; Peroxidase - metabolism ; Phosphatidylethanolamine Binding Protein - antagonists & inhibitors ; Platelet-derived growth factor ; Platelet-Derived Growth Factor - metabolism ; RNA, Messenger - metabolism ; Superoxide ; Tissue Inhibitor of Metalloproteinase-1 - genetics ; Tissue Inhibitor of Metalloproteinase-1 - metabolism ; Tissue Inhibitor of Metalloproteinase-2 - genetics ; Tissue Inhibitor of Metalloproteinase-2 - metabolism ; Transforming Growth Factor beta - metabolism ; Transforming growth factors ; Transplant Surgery</subject><ispartof>Digestive diseases and sciences, 2019-09, Vol.64 (9), p.2570-2580</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>COPYRIGHT 2019 Springer</rights><rights>Digestive Diseases and Sciences is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-ec65086c07ee37ac47c0a089dfde54a512551c6aaf4518ae0ec93999c1c9f8423</citedby><cites>FETCH-LOGICAL-c442t-ec65086c07ee37ac47c0a089dfde54a512551c6aaf4518ae0ec93999c1c9f8423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10620-019-05588-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10620-019-05588-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30874989$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Junji</creatorcontrib><creatorcontrib>Qiu, Yuzi</creatorcontrib><creatorcontrib>Wang, Min</creatorcontrib><creatorcontrib>Zhang, Ming</creatorcontrib><creatorcontrib>Zhao, Xiaoyi</creatorcontrib><creatorcontrib>Jiang, Huiqing</creatorcontrib><title>Locostatin Alleviates Liver Fibrosis Induced by Carbon Tetrachloride in Mice</title><title>Digestive diseases and sciences</title><addtitle>Dig Dis Sci</addtitle><addtitle>Dig Dis Sci</addtitle><description>Background and Aims
Liver fibrosis is featured with excessive deposition of extracellular matrix and fibrous connective tissue hyperplasia. The specific inhibitor of Raf-1 kinase inhibitor protein, locostatin, inhibits the migration of hepatic stellate cells. In this study, we investigated the effect of locostatin on liver fibrosis and its underlying mechanism.
Methods
Carbon tetrachloride (CCl4) was used to induce liver fibrosis in mice, and locostatin was injected intraperitoneally. Liver fibrosis was assessed by Masson and Sirius red staining, hydroxyproline (HYP) assay, and collagen percentage area. Collagen I, collagen III, and α-SMA were detected by RT-PCR and western blot. The levels of MMP-13, MMP-2, TIMP-1, and TIMP-2 were estimated by ELISA. Liver inflammation was evaluated by HE staining and immunohistochemistry; liver myeloperoxidase (MPO), superoxide dismutase, and malondialdehyde were measured by ELISA; and cytokines were by Mouse Cytokine Array Q4000.
Results
Compared to the CCl4 group, HYP (208.56 ± 6.12) µg/g, percentage of total collagen at overall region (1.91 ± 0.13), MMP-13/TIMP-1 (0.19 ± 0.01), MPO (1.45 ± 0.04) U/g, TGF-β (2652 ± 91.20), PDGF-AA (3897 ± 290.69), and E-selectin (1569 ± 66.48) in the liver tissues were decreased significantly in the locostatin-treated group.
Conclusions
Locostatin mitigated liver fibrosis and inflammation induced by CCl4. The mechanism is via inhibition inflammatory cytokines, TGF-β, PDGF-AA, and E-selectin.</description><subject>Actins - genetics</subject><subject>Actins - metabolism</subject><subject>Animals</subject><subject>Bile</subject><subject>Biochemistry</subject><subject>Carbon Tetrachloride</subject><subject>Cell Movement - drug effects</subject><subject>Collagen</subject><subject>Collagen Type I - genetics</subject><subject>Collagen Type I - metabolism</subject><subject>Collagen Type II - genetics</subject><subject>Collagen Type II - metabolism</subject><subject>Cytokines</subject><subject>E-Selectin - metabolism</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fibrosis</subject><subject>Gastroenterology</subject><subject>Hepatic Stellate Cells - physiology</subject><subject>Hepatology</subject><subject>Hydroxyproline - metabolism</subject><subject>Hyperplasia</subject><subject>Liver</subject><subject>Liver Cirrhosis - chemically induced</subject><subject>Liver Cirrhosis - drug therapy</subject><subject>Liver Cirrhosis - metabolism</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver diseases</subject><subject>Male</subject><subject>Matrix Metalloproteinase 13 - genetics</subject><subject>Matrix Metalloproteinase 13 - metabolism</subject><subject>Matrix Metalloproteinase 2 - genetics</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Oxazolidinones - pharmacology</subject><subject>Oxazolidinones - therapeutic use</subject><subject>Peroxidase - metabolism</subject><subject>Phosphatidylethanolamine Binding Protein - antagonists & inhibitors</subject><subject>Platelet-derived growth factor</subject><subject>Platelet-Derived Growth Factor - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Superoxide</subject><subject>Tissue Inhibitor of Metalloproteinase-1 - genetics</subject><subject>Tissue Inhibitor of Metalloproteinase-1 - metabolism</subject><subject>Tissue Inhibitor of Metalloproteinase-2 - genetics</subject><subject>Tissue Inhibitor of Metalloproteinase-2 - metabolism</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Transforming growth factors</subject><subject>Transplant Surgery</subject><issn>0163-2116</issn><issn>1573-2568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kU9v1DAQxS0EotvCF-CAInHhkjITx_-OqxWFSkFcytnyOpPiKhsXO6nUb4_DllYghHywNf69p5l5jL1BOEcA9SEjyAZqQFODEFrX4hnboFC8boTUz9kGUJY3ojxhpznfAIBRKF-yEw5atUabDeu66GOe3RymajuOdBfcTLnqwh2l6iLsU8whV5dTv3jqq_19tXNpH6fqiubk_PcxptBTVcRfgqdX7MXgxkyvH-4z9u3i49Xuc919_XS523a1b9tmrslLAVp6UERcOd8qDw606YeeROsENkKgl84NrUDtCMgbbozx6M2g24afsfdH39sUfyyUZ3sI2dM4uonikm2DhqPUqFVB3_2F3sQlTaW7lcKGC6ngibp2I9kwDXGdbjW1W4WN4ZIbUajzf1Dl9HQIPk40hFL_Q9AcBb6sMSca7G0KB5fuLYJdI7THCG2J0P6K0K6itw8dL_sD9Y-S35kVgB-BXL6ma0pPI_3H9ic54qPo</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Ma, Junji</creator><creator>Qiu, Yuzi</creator><creator>Wang, Min</creator><creator>Zhang, Ming</creator><creator>Zhao, Xiaoyi</creator><creator>Jiang, Huiqing</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20190901</creationdate><title>Locostatin Alleviates Liver Fibrosis Induced by Carbon Tetrachloride in Mice</title><author>Ma, Junji ; Qiu, Yuzi ; Wang, Min ; Zhang, Ming ; Zhao, Xiaoyi ; Jiang, Huiqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-ec65086c07ee37ac47c0a089dfde54a512551c6aaf4518ae0ec93999c1c9f8423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Actins - genetics</topic><topic>Actins - metabolism</topic><topic>Animals</topic><topic>Bile</topic><topic>Biochemistry</topic><topic>Carbon Tetrachloride</topic><topic>Cell Movement - drug effects</topic><topic>Collagen</topic><topic>Collagen Type I - genetics</topic><topic>Collagen Type I - metabolism</topic><topic>Collagen Type II - genetics</topic><topic>Collagen Type II - metabolism</topic><topic>Cytokines</topic><topic>E-Selectin - metabolism</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Fibrosis</topic><topic>Gastroenterology</topic><topic>Hepatic Stellate Cells - physiology</topic><topic>Hepatology</topic><topic>Hydroxyproline - metabolism</topic><topic>Hyperplasia</topic><topic>Liver</topic><topic>Liver Cirrhosis - chemically induced</topic><topic>Liver Cirrhosis - drug therapy</topic><topic>Liver Cirrhosis - metabolism</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver diseases</topic><topic>Male</topic><topic>Matrix Metalloproteinase 13 - genetics</topic><topic>Matrix Metalloproteinase 13 - metabolism</topic><topic>Matrix Metalloproteinase 2 - genetics</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Oxazolidinones - pharmacology</topic><topic>Oxazolidinones - therapeutic use</topic><topic>Peroxidase - metabolism</topic><topic>Phosphatidylethanolamine Binding Protein - antagonists & inhibitors</topic><topic>Platelet-derived growth factor</topic><topic>Platelet-Derived Growth Factor - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Superoxide</topic><topic>Tissue Inhibitor of Metalloproteinase-1 - genetics</topic><topic>Tissue Inhibitor of Metalloproteinase-1 - metabolism</topic><topic>Tissue Inhibitor of Metalloproteinase-2 - genetics</topic><topic>Tissue Inhibitor of Metalloproteinase-2 - metabolism</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Transforming growth factors</topic><topic>Transplant Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Junji</creatorcontrib><creatorcontrib>Qiu, Yuzi</creatorcontrib><creatorcontrib>Wang, Min</creatorcontrib><creatorcontrib>Zhang, Ming</creatorcontrib><creatorcontrib>Zhao, Xiaoyi</creatorcontrib><creatorcontrib>Jiang, Huiqing</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>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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><jtitle>Digestive diseases and sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Junji</au><au>Qiu, Yuzi</au><au>Wang, Min</au><au>Zhang, Ming</au><au>Zhao, Xiaoyi</au><au>Jiang, Huiqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Locostatin Alleviates Liver Fibrosis Induced by Carbon Tetrachloride in Mice</atitle><jtitle>Digestive diseases and sciences</jtitle><stitle>Dig Dis Sci</stitle><addtitle>Dig Dis Sci</addtitle><date>2019-09-01</date><risdate>2019</risdate><volume>64</volume><issue>9</issue><spage>2570</spage><epage>2580</epage><pages>2570-2580</pages><issn>0163-2116</issn><eissn>1573-2568</eissn><abstract>Background and Aims
Liver fibrosis is featured with excessive deposition of extracellular matrix and fibrous connective tissue hyperplasia. The specific inhibitor of Raf-1 kinase inhibitor protein, locostatin, inhibits the migration of hepatic stellate cells. In this study, we investigated the effect of locostatin on liver fibrosis and its underlying mechanism.
Methods
Carbon tetrachloride (CCl4) was used to induce liver fibrosis in mice, and locostatin was injected intraperitoneally. Liver fibrosis was assessed by Masson and Sirius red staining, hydroxyproline (HYP) assay, and collagen percentage area. Collagen I, collagen III, and α-SMA were detected by RT-PCR and western blot. The levels of MMP-13, MMP-2, TIMP-1, and TIMP-2 were estimated by ELISA. Liver inflammation was evaluated by HE staining and immunohistochemistry; liver myeloperoxidase (MPO), superoxide dismutase, and malondialdehyde were measured by ELISA; and cytokines were by Mouse Cytokine Array Q4000.
Results
Compared to the CCl4 group, HYP (208.56 ± 6.12) µg/g, percentage of total collagen at overall region (1.91 ± 0.13), MMP-13/TIMP-1 (0.19 ± 0.01), MPO (1.45 ± 0.04) U/g, TGF-β (2652 ± 91.20), PDGF-AA (3897 ± 290.69), and E-selectin (1569 ± 66.48) in the liver tissues were decreased significantly in the locostatin-treated group.
Conclusions
Locostatin mitigated liver fibrosis and inflammation induced by CCl4. The mechanism is via inhibition inflammatory cytokines, TGF-β, PDGF-AA, and E-selectin.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30874989</pmid><doi>10.1007/s10620-019-05588-5</doi><tpages>11</tpages></addata></record> |
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| subjects | Actins - genetics Actins - metabolism Animals Bile Biochemistry Carbon Tetrachloride Cell Movement - drug effects Collagen Collagen Type I - genetics Collagen Type I - metabolism Collagen Type II - genetics Collagen Type II - metabolism Cytokines E-Selectin - metabolism Enzyme-linked immunosorbent assay Fibrosis Gastroenterology Hepatic Stellate Cells - physiology Hepatology Hydroxyproline - metabolism Hyperplasia Liver Liver Cirrhosis - chemically induced Liver Cirrhosis - drug therapy Liver Cirrhosis - metabolism Liver Cirrhosis - pathology Liver diseases Male Matrix Metalloproteinase 13 - genetics Matrix Metalloproteinase 13 - metabolism Matrix Metalloproteinase 2 - genetics Matrix Metalloproteinase 2 - metabolism Medicine Medicine & Public Health Mice Mice, Inbred C57BL Oncology Original Article Oxazolidinones - pharmacology Oxazolidinones - therapeutic use Peroxidase - metabolism Phosphatidylethanolamine Binding Protein - antagonists & inhibitors Platelet-derived growth factor Platelet-Derived Growth Factor - metabolism RNA, Messenger - metabolism Superoxide Tissue Inhibitor of Metalloproteinase-1 - genetics Tissue Inhibitor of Metalloproteinase-1 - metabolism Tissue Inhibitor of Metalloproteinase-2 - genetics Tissue Inhibitor of Metalloproteinase-2 - metabolism Transforming Growth Factor beta - metabolism Transforming growth factors Transplant Surgery |
| title | Locostatin Alleviates Liver Fibrosis Induced by Carbon Tetrachloride in Mice |
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