Celastrol exerts anti‐inflammatory effect in liver fibrosis via activation of AMPK‐SIRT3 signalling
Celastrol, a pentacyclic tritepene extracted from Tripterygium Wilfordi plant, showing potent liver protection effects on several liver‐related diseases. However, the anti‐inflammatory potential of celastrol in liver fibrosis and the detailed mechanisms remain uncovered. This study was to investigat...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2020-01, Vol.24 (1), p.941-953 |
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| creator | Wang, Yuqin Li, Chunling Gu, Jingya Chen, Chang Duanmu, Jiaxin Miao, Jing Yao, Wenjuan Tao, Jinhua Tu, Mengjue Xiong, Biao Zhao, Lingling Liu, Zhaoguo |
| description | Celastrol, a pentacyclic tritepene extracted from Tripterygium Wilfordi plant, showing potent liver protection effects on several liver‐related diseases. However, the anti‐inflammatory potential of celastrol in liver fibrosis and the detailed mechanisms remain uncovered. This study was to investigate the anti‐inflammatory effect of celastrol in liver fibrosis and to further reveal mechanisms of celastrol‐induced anti‐inflammatory effects with a focus on AMPK‐SIRT3 signalling. Celastrol showed potent ameliorative effects on liver fibrosis both in activated hepatic stellate cells (HSCs) and in fibrotic liver. Celastrol remarkably suppressed inflammation in vivo and inhibited the secretion of inflammatory factors in vitro. Interestingly, celastrol increased SIRT3 promoter activity and SIRT3 expression both in fibrotic liver and in activated HSCs. Furthermore, SIRT3 silencing evidently ameliorated the anti‐inflammatory potential of celastrol. Besides, we found that celastrol could increase the AMPK phosphorylation. Further investigation showed that SIRT3 siRNA decreased SIRT3 expression but had no obvious effect on phosphorylation of AMPK. In addition, inhibition of AMPK by employing compound C (an AMPK inhibitor) or AMPK1α siRNA significantly suppressed SIRT3 expression, suggesting that AMPK was an up‐stream protein of SIRT3 in liver fibrosis. We further found that depletion of AMPK significantly attenuated the inhibitory effect of celastrol on inflammation. Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK‐SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis. |
| doi_str_mv | 10.1111/jcmm.14805 |
| format | Article |
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However, the anti‐inflammatory potential of celastrol in liver fibrosis and the detailed mechanisms remain uncovered. This study was to investigate the anti‐inflammatory effect of celastrol in liver fibrosis and to further reveal mechanisms of celastrol‐induced anti‐inflammatory effects with a focus on AMPK‐SIRT3 signalling. Celastrol showed potent ameliorative effects on liver fibrosis both in activated hepatic stellate cells (HSCs) and in fibrotic liver. Celastrol remarkably suppressed inflammation in vivo and inhibited the secretion of inflammatory factors in vitro. Interestingly, celastrol increased SIRT3 promoter activity and SIRT3 expression both in fibrotic liver and in activated HSCs. Furthermore, SIRT3 silencing evidently ameliorated the anti‐inflammatory potential of celastrol. Besides, we found that celastrol could increase the AMPK phosphorylation. Further investigation showed that SIRT3 siRNA decreased SIRT3 expression but had no obvious effect on phosphorylation of AMPK. In addition, inhibition of AMPK by employing compound C (an AMPK inhibitor) or AMPK1α siRNA significantly suppressed SIRT3 expression, suggesting that AMPK was an up‐stream protein of SIRT3 in liver fibrosis. We further found that depletion of AMPK significantly attenuated the inhibitory effect of celastrol on inflammation. Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK‐SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.14805</identifier><identifier>PMID: 31742890</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>AMP-Activated Protein Kinases - genetics ; AMP-Activated Protein Kinases - metabolism ; AMPK ; Animals ; Anti-Inflammatory Agents - pharmacology ; Bile ; Bioengineering ; celastrol ; Cell cycle ; Chinese medicine ; Cytokines ; Cytotoxicity ; Depletion ; Disease ; Enzymes ; Experiments ; Fibrosis ; Gene Expression Regulation - drug effects ; Hepatic Stellate Cells - drug effects ; Hepatic Stellate Cells - immunology ; Hepatic Stellate Cells - metabolism ; Inflammation ; Inflammation - drug therapy ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation - pathology ; Laboratory animals ; Liver ; Liver Cirrhosis - drug therapy ; Liver Cirrhosis - immunology ; Liver Cirrhosis - metabolism ; Liver Cirrhosis - pathology ; Liver diseases ; liver fibrosis ; Male ; Medical research ; Olive oil ; Original ; Pentacyclic Triterpenes - pharmacology ; Phosphorylation ; Plant extracts ; Plant protection ; Proteins ; Protocol ; Rats ; Rats, Sprague-Dawley ; Reagents ; siRNA ; SIRT3 ; Sirtuins - genetics ; Sirtuins - metabolism ; Stellate cells ; Tumor necrosis factor-TNF</subject><ispartof>Journal of cellular and molecular medicine, 2020-01, Vol.24 (1), p.941-953</ispartof><rights>2019 The Authors. published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2020. 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-c4765-48e433810ca80738688d5b08c2014793d3ce8bec5d423e195894f5b1906378c33</citedby><cites>FETCH-LOGICAL-c4765-48e433810ca80738688d5b08c2014793d3ce8bec5d423e195894f5b1906378c33</cites><orcidid>0000-0001-6311-8338</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6933398/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6933398/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11561,27923,27924,45573,45574,46051,46475,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31742890$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yuqin</creatorcontrib><creatorcontrib>Li, Chunling</creatorcontrib><creatorcontrib>Gu, Jingya</creatorcontrib><creatorcontrib>Chen, Chang</creatorcontrib><creatorcontrib>Duanmu, Jiaxin</creatorcontrib><creatorcontrib>Miao, Jing</creatorcontrib><creatorcontrib>Yao, Wenjuan</creatorcontrib><creatorcontrib>Tao, Jinhua</creatorcontrib><creatorcontrib>Tu, Mengjue</creatorcontrib><creatorcontrib>Xiong, Biao</creatorcontrib><creatorcontrib>Zhao, Lingling</creatorcontrib><creatorcontrib>Liu, Zhaoguo</creatorcontrib><title>Celastrol exerts anti‐inflammatory effect in liver fibrosis via activation of AMPK‐SIRT3 signalling</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Celastrol, a pentacyclic tritepene extracted from Tripterygium Wilfordi plant, showing potent liver protection effects on several liver‐related diseases. However, the anti‐inflammatory potential of celastrol in liver fibrosis and the detailed mechanisms remain uncovered. This study was to investigate the anti‐inflammatory effect of celastrol in liver fibrosis and to further reveal mechanisms of celastrol‐induced anti‐inflammatory effects with a focus on AMPK‐SIRT3 signalling. Celastrol showed potent ameliorative effects on liver fibrosis both in activated hepatic stellate cells (HSCs) and in fibrotic liver. Celastrol remarkably suppressed inflammation in vivo and inhibited the secretion of inflammatory factors in vitro. Interestingly, celastrol increased SIRT3 promoter activity and SIRT3 expression both in fibrotic liver and in activated HSCs. Furthermore, SIRT3 silencing evidently ameliorated the anti‐inflammatory potential of celastrol. Besides, we found that celastrol could increase the AMPK phosphorylation. Further investigation showed that SIRT3 siRNA decreased SIRT3 expression but had no obvious effect on phosphorylation of AMPK. In addition, inhibition of AMPK by employing compound C (an AMPK inhibitor) or AMPK1α siRNA significantly suppressed SIRT3 expression, suggesting that AMPK was an up‐stream protein of SIRT3 in liver fibrosis. We further found that depletion of AMPK significantly attenuated the inhibitory effect of celastrol on inflammation. Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK‐SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis.</description><subject>AMP-Activated Protein Kinases - genetics</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>AMPK</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Bile</subject><subject>Bioengineering</subject><subject>celastrol</subject><subject>Cell cycle</subject><subject>Chinese medicine</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Depletion</subject><subject>Disease</subject><subject>Enzymes</subject><subject>Experiments</subject><subject>Fibrosis</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hepatic Stellate Cells - drug effects</subject><subject>Hepatic Stellate Cells - immunology</subject><subject>Hepatic Stellate Cells - metabolism</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Laboratory animals</subject><subject>Liver</subject><subject>Liver Cirrhosis - drug therapy</subject><subject>Liver Cirrhosis - immunology</subject><subject>Liver Cirrhosis - metabolism</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver diseases</subject><subject>liver fibrosis</subject><subject>Male</subject><subject>Medical research</subject><subject>Olive oil</subject><subject>Original</subject><subject>Pentacyclic Triterpenes - pharmacology</subject><subject>Phosphorylation</subject><subject>Plant extracts</subject><subject>Plant protection</subject><subject>Proteins</subject><subject>Protocol</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reagents</subject><subject>siRNA</subject><subject>SIRT3</subject><subject>Sirtuins - genetics</subject><subject>Sirtuins - metabolism</subject><subject>Stellate cells</subject><subject>Tumor necrosis factor-TNF</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><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>eNp9kd1uFCEYhidGY3_0xAswJJ4Yk60wH8x8nJg0G3-q3Wi0HhOGZVY2zFCBXbtnXoLX2Csp666NelBOIOHhgZe3qp4wesLKeLk0w3DCOFJxrzpkAusJl8Dv79cMAQ-qo5SWlELDQD6sDoC1vEZJD6vF1Hqdcgye2CsbcyJ6zO765y839l4Pg84hbojte2sycSPxbm0j6V0XQ3KJrJ0m2mS31tmFkYSenM4-fSjHv5x9vgCS3GLU3rtx8ah60Guf7OP9fFx9ffP6Yvpucv7x7dn09HxieNuICUfLAZBRo5G2gA3iXHQUTU0ZbyXMwVjsrBFzXoNlUqDkveiYpA20aACOq1c77-WqG-zc2DFH7dVldIOOGxW0U__ujO6bWoS1aiQASCyC53tBDN9XNmU1uGSs93q0YZVUDUzIBhvY3vXsP3QZVrEELpSoBWJJ0txJAZSQTEpZqBc7ypSPTdH2t09mVG1bVtuW1e-WC_z075C36J9aC8B2wA_n7eYOlXo_nc120htooLM4</recordid><startdate>202001</startdate><enddate>202001</enddate><creator>Wang, Yuqin</creator><creator>Li, Chunling</creator><creator>Gu, Jingya</creator><creator>Chen, Chang</creator><creator>Duanmu, Jiaxin</creator><creator>Miao, Jing</creator><creator>Yao, Wenjuan</creator><creator>Tao, Jinhua</creator><creator>Tu, Mengjue</creator><creator>Xiong, Biao</creator><creator>Zhao, Lingling</creator><creator>Liu, Zhaoguo</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6311-8338</orcidid></search><sort><creationdate>202001</creationdate><title>Celastrol exerts anti‐inflammatory effect in liver fibrosis via activation of AMPK‐SIRT3 signalling</title><author>Wang, Yuqin ; Li, Chunling ; Gu, Jingya ; Chen, Chang ; Duanmu, Jiaxin ; Miao, Jing ; Yao, Wenjuan ; Tao, Jinhua ; Tu, Mengjue ; Xiong, Biao ; Zhao, Lingling ; Liu, Zhaoguo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4765-48e433810ca80738688d5b08c2014793d3ce8bec5d423e195894f5b1906378c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>AMP-Activated Protein Kinases - genetics</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>AMPK</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Bile</topic><topic>Bioengineering</topic><topic>celastrol</topic><topic>Cell cycle</topic><topic>Chinese medicine</topic><topic>Cytokines</topic><topic>Cytotoxicity</topic><topic>Depletion</topic><topic>Disease</topic><topic>Enzymes</topic><topic>Experiments</topic><topic>Fibrosis</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Hepatic Stellate Cells - drug effects</topic><topic>Hepatic Stellate Cells - immunology</topic><topic>Hepatic Stellate Cells - metabolism</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - immunology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Laboratory animals</topic><topic>Liver</topic><topic>Liver Cirrhosis - drug therapy</topic><topic>Liver Cirrhosis - immunology</topic><topic>Liver Cirrhosis - metabolism</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver diseases</topic><topic>liver fibrosis</topic><topic>Male</topic><topic>Medical research</topic><topic>Olive oil</topic><topic>Original</topic><topic>Pentacyclic Triterpenes - pharmacology</topic><topic>Phosphorylation</topic><topic>Plant extracts</topic><topic>Plant protection</topic><topic>Proteins</topic><topic>Protocol</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reagents</topic><topic>siRNA</topic><topic>SIRT3</topic><topic>Sirtuins - genetics</topic><topic>Sirtuins - metabolism</topic><topic>Stellate cells</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yuqin</creatorcontrib><creatorcontrib>Li, Chunling</creatorcontrib><creatorcontrib>Gu, Jingya</creatorcontrib><creatorcontrib>Chen, Chang</creatorcontrib><creatorcontrib>Duanmu, Jiaxin</creatorcontrib><creatorcontrib>Miao, Jing</creatorcontrib><creatorcontrib>Yao, Wenjuan</creatorcontrib><creatorcontrib>Tao, Jinhua</creatorcontrib><creatorcontrib>Tu, Mengjue</creatorcontrib><creatorcontrib>Xiong, Biao</creatorcontrib><creatorcontrib>Zhao, Lingling</creatorcontrib><creatorcontrib>Liu, Zhaoguo</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>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>Biotechnology and BioEngineering Abstracts</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><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yuqin</au><au>Li, Chunling</au><au>Gu, Jingya</au><au>Chen, Chang</au><au>Duanmu, Jiaxin</au><au>Miao, Jing</au><au>Yao, Wenjuan</au><au>Tao, Jinhua</au><au>Tu, Mengjue</au><au>Xiong, Biao</au><au>Zhao, Lingling</au><au>Liu, Zhaoguo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Celastrol exerts anti‐inflammatory effect in liver fibrosis via activation of AMPK‐SIRT3 signalling</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2020-01</date><risdate>2020</risdate><volume>24</volume><issue>1</issue><spage>941</spage><epage>953</epage><pages>941-953</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Celastrol, a pentacyclic tritepene extracted from Tripterygium Wilfordi plant, showing potent liver protection effects on several liver‐related diseases. However, the anti‐inflammatory potential of celastrol in liver fibrosis and the detailed mechanisms remain uncovered. This study was to investigate the anti‐inflammatory effect of celastrol in liver fibrosis and to further reveal mechanisms of celastrol‐induced anti‐inflammatory effects with a focus on AMPK‐SIRT3 signalling. Celastrol showed potent ameliorative effects on liver fibrosis both in activated hepatic stellate cells (HSCs) and in fibrotic liver. Celastrol remarkably suppressed inflammation in vivo and inhibited the secretion of inflammatory factors in vitro. Interestingly, celastrol increased SIRT3 promoter activity and SIRT3 expression both in fibrotic liver and in activated HSCs. Furthermore, SIRT3 silencing evidently ameliorated the anti‐inflammatory potential of celastrol. Besides, we found that celastrol could increase the AMPK phosphorylation. Further investigation showed that SIRT3 siRNA decreased SIRT3 expression but had no obvious effect on phosphorylation of AMPK. In addition, inhibition of AMPK by employing compound C (an AMPK inhibitor) or AMPK1α siRNA significantly suppressed SIRT3 expression, suggesting that AMPK was an up‐stream protein of SIRT3 in liver fibrosis. We further found that depletion of AMPK significantly attenuated the inhibitory effect of celastrol on inflammation. Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK‐SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>31742890</pmid><doi>10.1111/jcmm.14805</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-6311-8338</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | AMP-Activated Protein Kinases - genetics AMP-Activated Protein Kinases - metabolism AMPK Animals Anti-Inflammatory Agents - pharmacology Bile Bioengineering celastrol Cell cycle Chinese medicine Cytokines Cytotoxicity Depletion Disease Enzymes Experiments Fibrosis Gene Expression Regulation - drug effects Hepatic Stellate Cells - drug effects Hepatic Stellate Cells - immunology Hepatic Stellate Cells - metabolism Inflammation Inflammation - drug therapy Inflammation - immunology Inflammation - metabolism Inflammation - pathology Laboratory animals Liver Liver Cirrhosis - drug therapy Liver Cirrhosis - immunology Liver Cirrhosis - metabolism Liver Cirrhosis - pathology Liver diseases liver fibrosis Male Medical research Olive oil Original Pentacyclic Triterpenes - pharmacology Phosphorylation Plant extracts Plant protection Proteins Protocol Rats Rats, Sprague-Dawley Reagents siRNA SIRT3 Sirtuins - genetics Sirtuins - metabolism Stellate cells Tumor necrosis factor-TNF |
| title | Celastrol exerts anti‐inflammatory effect in liver fibrosis via activation of AMPK‐SIRT3 signalling |
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