Ferulic acid attenuates ischemia/reperfusion-induced hepatocyte apoptosis via inhibition of JNK activation
Ferulic acid (FA), a phenolic compound found in various medicinal plants, has hepatoprotective effects against oxidative stress and inflammation. Here, we investigated the protective effects and the specific mechanisms of FA against hepatocyte apoptosis caused by ischemia/reperfusion (I/R). Mice wer...
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| Veröffentlicht in: | European journal of pharmaceutical sciences 2012-04, Vol.45 (5), p.708-715 |
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| description | Ferulic acid (FA), a phenolic compound found in various medicinal plants, has hepatoprotective effects against oxidative stress and inflammation. Here, we investigated the protective effects and the specific mechanisms of FA against hepatocyte apoptosis caused by ischemia/reperfusion (I/R). Mice were treated intraperitoneally with vehicle or FA 30min prior to 60min of ischemia. After 5h of reperfusion, serum aminotransferase activities and hepatic lipid peroxidation were elevated and hepatic glutathione content was depleted. These alterations were attenuated by FA. I/R increased caspase-3 activity and release of cytochrome c, and these were suppressed by FA. FA also attenuated the increases in the serum tumor necrosis factor (TNF)-α levels and TNF receptor type 1-associated DEATH domain protein and TNF receptor-associated factor 2 protein expressions. The cytosolic levels of Bcl-2-associated X protein (Bax), truncated BH3 interacting domain death agonist (tBid), and Bcl-2-like protein 11 were upregulated after reperfusion. The increases in Bax and tBid protein expression were attenuated by FA. Moreover, I/R induced c-Jun N-terminal kinase 1 (JNK1) and JNK2 phosphorylation, and FA attenuated the JNK activation. FA protects against I/R-induced hepatocyte apoptosis by attenuating oxidative stress and JNK activation. |
| doi_str_mv | 10.1016/j.ejps.2012.01.010 |
| format | Article |
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Here, we investigated the protective effects and the specific mechanisms of FA against hepatocyte apoptosis caused by ischemia/reperfusion (I/R). Mice were treated intraperitoneally with vehicle or FA 30min prior to 60min of ischemia. After 5h of reperfusion, serum aminotransferase activities and hepatic lipid peroxidation were elevated and hepatic glutathione content was depleted. These alterations were attenuated by FA. I/R increased caspase-3 activity and release of cytochrome c, and these were suppressed by FA. FA also attenuated the increases in the serum tumor necrosis factor (TNF)-α levels and TNF receptor type 1-associated DEATH domain protein and TNF receptor-associated factor 2 protein expressions. The cytosolic levels of Bcl-2-associated X protein (Bax), truncated BH3 interacting domain death agonist (tBid), and Bcl-2-like protein 11 were upregulated after reperfusion. The increases in Bax and tBid protein expression were attenuated by FA. Moreover, I/R induced c-Jun N-terminal kinase 1 (JNK1) and JNK2 phosphorylation, and FA attenuated the JNK activation. FA protects against I/R-induced hepatocyte apoptosis by attenuating oxidative stress and JNK activation.</description><identifier>ISSN: 0928-0987</identifier><identifier>EISSN: 1879-0720</identifier><identifier>DOI: 10.1016/j.ejps.2012.01.010</identifier><identifier>PMID: 22326704</identifier><language>eng</language><publisher>Kindlington: Elsevier B.V</publisher><subject>Animals ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Apoptosis Regulatory Proteins - genetics ; Apoptosis Regulatory Proteins - metabolism ; bcl-2-Associated X Protein - genetics ; bcl-2-Associated X Protein - metabolism ; Bcl-2-Like Protein 11 ; BH3 Interacting Domain Death Agonist Protein - genetics ; BH3 Interacting Domain Death Agonist Protein - metabolism ; Biological and medical sciences ; Caspase 3 - genetics ; Caspase 3 - metabolism ; Caspase 8 - genetics ; Caspase 8 - metabolism ; Coumaric Acids - pharmacology ; Cytochromes c - genetics ; Cytochromes c - metabolism ; Cytosol - drug effects ; Cytosol - metabolism ; Ferulic acid ; General pharmacology ; Glutathione - genetics ; Glutathione - metabolism ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; Ischemia/reperfusion ; Lipid Peroxidation - drug effects ; Liver ; Liver - blood supply ; Liver - drug effects ; Liver - metabolism ; Male ; MAP Kinase Kinase 4 - antagonists & inhibitors ; MAP Kinase Kinase 4 - genetics ; MAP Kinase Kinase 4 - metabolism ; Medical sciences ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred ICR ; Oxidative stress ; Oxidative Stress - drug effects ; Pharmaceutical technology. Pharmaceutical industry ; Pharmacology. Drug treatments ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; Reperfusion Injury - drug therapy ; Reperfusion Injury - genetics ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Signal Transduction - drug effects ; TNF Receptor-Associated Death Domain Protein - genetics ; TNF Receptor-Associated Death Domain Protein - metabolism ; TNF Receptor-Associated Factor 2 - genetics ; TNF Receptor-Associated Factor 2 - metabolism ; Transaminases - blood ; Tumor Necrosis Factor-alpha - blood ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Up-Regulation - drug effects ; Up-Regulation - genetics</subject><ispartof>European journal of pharmaceutical sciences, 2012-04, Vol.45 (5), p.708-715</ispartof><rights>2012 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-ec92e5333141a03923744d7b5a3cf734b4ad584fa4ba42b3842d7662521688fa3</citedby><cites>FETCH-LOGICAL-c451t-ec92e5333141a03923744d7b5a3cf734b4ad584fa4ba42b3842d7662521688fa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S092809871200053X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25609452$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22326704$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Hyo-Yeon</creatorcontrib><creatorcontrib>Lee, Sun-Mee</creatorcontrib><title>Ferulic acid attenuates ischemia/reperfusion-induced hepatocyte apoptosis via inhibition of JNK activation</title><title>European journal of pharmaceutical sciences</title><addtitle>Eur J Pharm Sci</addtitle><description>Ferulic acid (FA), a phenolic compound found in various medicinal plants, has hepatoprotective effects against oxidative stress and inflammation. Here, we investigated the protective effects and the specific mechanisms of FA against hepatocyte apoptosis caused by ischemia/reperfusion (I/R). Mice were treated intraperitoneally with vehicle or FA 30min prior to 60min of ischemia. After 5h of reperfusion, serum aminotransferase activities and hepatic lipid peroxidation were elevated and hepatic glutathione content was depleted. These alterations were attenuated by FA. I/R increased caspase-3 activity and release of cytochrome c, and these were suppressed by FA. FA also attenuated the increases in the serum tumor necrosis factor (TNF)-α levels and TNF receptor type 1-associated DEATH domain protein and TNF receptor-associated factor 2 protein expressions. The cytosolic levels of Bcl-2-associated X protein (Bax), truncated BH3 interacting domain death agonist (tBid), and Bcl-2-like protein 11 were upregulated after reperfusion. The increases in Bax and tBid protein expression were attenuated by FA. Moreover, I/R induced c-Jun N-terminal kinase 1 (JNK1) and JNK2 phosphorylation, and FA attenuated the JNK activation. FA protects against I/R-induced hepatocyte apoptosis by attenuating oxidative stress and JNK activation.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>bcl-2-Associated X Protein - genetics</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Bcl-2-Like Protein 11</subject><subject>BH3 Interacting Domain Death Agonist Protein - genetics</subject><subject>BH3 Interacting Domain Death Agonist Protein - metabolism</subject><subject>Biological and medical sciences</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase 8 - genetics</subject><subject>Caspase 8 - metabolism</subject><subject>Coumaric Acids - pharmacology</subject><subject>Cytochromes c - genetics</subject><subject>Cytochromes c - metabolism</subject><subject>Cytosol - drug effects</subject><subject>Cytosol - metabolism</subject><subject>Ferulic acid</subject><subject>General pharmacology</subject><subject>Glutathione - genetics</subject><subject>Glutathione - metabolism</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>Ischemia/reperfusion</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Liver</subject><subject>Liver - blood supply</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>MAP Kinase Kinase 4 - antagonists & inhibitors</subject><subject>MAP Kinase Kinase 4 - genetics</subject><subject>MAP Kinase Kinase 4 - metabolism</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pharmaceutical technology. Pharmaceutical industry</subject><subject>Pharmacology. Drug treatments</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - genetics</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Signal Transduction - drug effects</subject><subject>TNF Receptor-Associated Death Domain Protein - genetics</subject><subject>TNF Receptor-Associated Death Domain Protein - metabolism</subject><subject>TNF Receptor-Associated Factor 2 - genetics</subject><subject>TNF Receptor-Associated Factor 2 - metabolism</subject><subject>Transaminases - blood</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Up-Regulation - drug effects</subject><subject>Up-Regulation - genetics</subject><issn>0928-0987</issn><issn>1879-0720</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE2L1EAQhhtR3HH1D3iQvoinzFZ_JJ2AF1l2_Vr0ouem0qkwHTJJ7O4M7L-3w4x6EwoKiqdeqh7GXgvYCxDVzbCnYYl7CULuQeSCJ2wnatMUYCQ8ZTtoZF1AU5sr9iLGAQCq2sBzdiWlkpUBvWPDPYV19I6j8x3HlGhaMVHkProDHT3eBFoo9Gv081T4qVsddfxAC6bZPSbiuMxLmqOP_OSR--ngW58yy-eef_n2Necmf8Jt8pI963GM9OrSr9nP-7sft5-Kh-8fP99-eCicLkUqyDWSSqWU0AJBNVIZrTvTlqhcb5RuNXZlrXvULWrZqlrLzlSVLKWo6rpHdc3enXOXMP9aKSZ7zM_QOOJE8xptI6sSGqUhk_JMujDHGKi3S_BHDI9WgN0U28Fuiu2m2ILItS29ucSv7ZG6vyt_nGbg7QXA6HDsA07Ox39cWUGjS5m592eOsoyTp2Cj8zRlvz6QS7ab_f_u-A0ON5rr</recordid><startdate>20120411</startdate><enddate>20120411</enddate><creator>Kim, Hyo-Yeon</creator><creator>Lee, Sun-Mee</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>20120411</creationdate><title>Ferulic acid attenuates ischemia/reperfusion-induced hepatocyte apoptosis via inhibition of JNK activation</title><author>Kim, Hyo-Yeon ; Lee, Sun-Mee</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-ec92e5333141a03923744d7b5a3cf734b4ad584fa4ba42b3842d7662521688fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>bcl-2-Associated X Protein - genetics</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Bcl-2-Like Protein 11</topic><topic>BH3 Interacting Domain Death Agonist Protein - genetics</topic><topic>BH3 Interacting Domain Death Agonist Protein - metabolism</topic><topic>Biological and medical sciences</topic><topic>Caspase 3 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase 8 - genetics</topic><topic>Caspase 8 - metabolism</topic><topic>Coumaric Acids - pharmacology</topic><topic>Cytochromes c - genetics</topic><topic>Cytochromes c - metabolism</topic><topic>Cytosol - drug effects</topic><topic>Cytosol - metabolism</topic><topic>Ferulic acid</topic><topic>General pharmacology</topic><topic>Glutathione - genetics</topic><topic>Glutathione - metabolism</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>Ischemia/reperfusion</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Liver</topic><topic>Liver - blood supply</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>MAP Kinase Kinase 4 - antagonists & inhibitors</topic><topic>MAP Kinase Kinase 4 - genetics</topic><topic>MAP Kinase Kinase 4 - metabolism</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Pharmaceutical technology. Pharmaceutical industry</topic><topic>Pharmacology. Drug treatments</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - genetics</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Signal Transduction - drug effects</topic><topic>TNF Receptor-Associated Death Domain Protein - genetics</topic><topic>TNF Receptor-Associated Death Domain Protein - metabolism</topic><topic>TNF Receptor-Associated Factor 2 - genetics</topic><topic>TNF Receptor-Associated Factor 2 - metabolism</topic><topic>Transaminases - blood</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Up-Regulation - drug effects</topic><topic>Up-Regulation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Hyo-Yeon</creatorcontrib><creatorcontrib>Lee, Sun-Mee</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmaceutical sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Hyo-Yeon</au><au>Lee, Sun-Mee</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ferulic acid attenuates ischemia/reperfusion-induced hepatocyte apoptosis via inhibition of JNK activation</atitle><jtitle>European journal of pharmaceutical sciences</jtitle><addtitle>Eur J Pharm Sci</addtitle><date>2012-04-11</date><risdate>2012</risdate><volume>45</volume><issue>5</issue><spage>708</spage><epage>715</epage><pages>708-715</pages><issn>0928-0987</issn><eissn>1879-0720</eissn><abstract>Ferulic acid (FA), a phenolic compound found in various medicinal plants, has hepatoprotective effects against oxidative stress and inflammation. Here, we investigated the protective effects and the specific mechanisms of FA against hepatocyte apoptosis caused by ischemia/reperfusion (I/R). Mice were treated intraperitoneally with vehicle or FA 30min prior to 60min of ischemia. After 5h of reperfusion, serum aminotransferase activities and hepatic lipid peroxidation were elevated and hepatic glutathione content was depleted. These alterations were attenuated by FA. I/R increased caspase-3 activity and release of cytochrome c, and these were suppressed by FA. FA also attenuated the increases in the serum tumor necrosis factor (TNF)-α levels and TNF receptor type 1-associated DEATH domain protein and TNF receptor-associated factor 2 protein expressions. The cytosolic levels of Bcl-2-associated X protein (Bax), truncated BH3 interacting domain death agonist (tBid), and Bcl-2-like protein 11 were upregulated after reperfusion. The increases in Bax and tBid protein expression were attenuated by FA. Moreover, I/R induced c-Jun N-terminal kinase 1 (JNK1) and JNK2 phosphorylation, and FA attenuated the JNK activation. FA protects against I/R-induced hepatocyte apoptosis by attenuating oxidative stress and JNK activation.</abstract><cop>Kindlington</cop><pub>Elsevier B.V</pub><pmid>22326704</pmid><doi>10.1016/j.ejps.2012.01.010</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Apoptosis Apoptosis - drug effects Apoptosis - genetics Apoptosis Regulatory Proteins - genetics Apoptosis Regulatory Proteins - metabolism bcl-2-Associated X Protein - genetics bcl-2-Associated X Protein - metabolism Bcl-2-Like Protein 11 BH3 Interacting Domain Death Agonist Protein - genetics BH3 Interacting Domain Death Agonist Protein - metabolism Biological and medical sciences Caspase 3 - genetics Caspase 3 - metabolism Caspase 8 - genetics Caspase 8 - metabolism Coumaric Acids - pharmacology Cytochromes c - genetics Cytochromes c - metabolism Cytosol - drug effects Cytosol - metabolism Ferulic acid General pharmacology Glutathione - genetics Glutathione - metabolism Hepatocytes - drug effects Hepatocytes - metabolism Ischemia/reperfusion Lipid Peroxidation - drug effects Liver Liver - blood supply Liver - drug effects Liver - metabolism Male MAP Kinase Kinase 4 - antagonists & inhibitors MAP Kinase Kinase 4 - genetics MAP Kinase Kinase 4 - metabolism Medical sciences Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Inbred ICR Oxidative stress Oxidative Stress - drug effects Pharmaceutical technology. Pharmaceutical industry Pharmacology. Drug treatments Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Reperfusion Injury - drug therapy Reperfusion Injury - genetics Reperfusion Injury - metabolism Reperfusion Injury - pathology Signal Transduction - drug effects TNF Receptor-Associated Death Domain Protein - genetics TNF Receptor-Associated Death Domain Protein - metabolism TNF Receptor-Associated Factor 2 - genetics TNF Receptor-Associated Factor 2 - metabolism Transaminases - blood Tumor Necrosis Factor-alpha - blood Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Up-Regulation - drug effects Up-Regulation - genetics |
| title | Ferulic acid attenuates ischemia/reperfusion-induced hepatocyte apoptosis via inhibition of JNK activation |
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