Role of the sympathetic nervous system in carbon tetrachloride-induced hepatotoxicity and systemic inflammation
Carbon tetrachloride (CCl4) is widely used as an animal model of hepatotoxicity and the mechanisms have been arduously studied, however, the contribution of the sympathetic nervous system (SNS) in CCl4-induced acute hepatotoxicity remains controversial. It is also known that either CCl4 or SNS can a...
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| description | Carbon tetrachloride (CCl4) is widely used as an animal model of hepatotoxicity and the mechanisms have been arduously studied, however, the contribution of the sympathetic nervous system (SNS) in CCl4-induced acute hepatotoxicity remains controversial. It is also known that either CCl4 or SNS can affect systemic inflammatory responses. The aim of this study was to establish the effect of chemical sympathectomy with 6-hydroxydopamine (6-OHDA) in a mouse model of CCl4-induced acute hepatotoxicity and systemic inflammatory response. Mice exposed to CCl4 or vehicle were pretreated with 6-OHDA or saline. The serum levels of aminotransferases and alkaline phosphatase in the CCl4-poisoning mice with sympathetic denervation were significantly lower than those without sympathetic denervation. With sympathetic denervation, hepatocellular necrosis and fat infiltration induced by CCl4 were greatly decreased. Sympathetic denervation significantly attenuated CCl4-induced lipid peroxidation in liver and serum. Acute CCl4 intoxication showed increased expression of inflammatory cytokines/chemokines [eotaxin-2/CCL24, Fas ligand, interleukin (IL)-1α, IL-6, IL-12p40p70, monocyte chemoattractant protein-1 (MCP-1/CCL2), and tumor necrosis factor-α (TNF-α)], as well as decreased expression of granulocyte colony-stimulating factor and keratinocyte-derived chemokine. The overexpressed levels of IL-1α, IL-6, IL-12p40p70, MCP-1/CCL2, and TNF-α were attenuated by sympathetic denervation. Pretreatment with dexamethasone significantly reduced CCl4-induced hepatic injury. Collectively, this study demonstrates that the SNS plays an important role in CCl4-induced acute hepatotoxicity and systemic inflammation and the effect may be connected with chemical- or drug-induced hepatotoxicity and circulating immune response. |
| doi_str_mv | 10.1371/journal.pone.0121365 |
| format | Article |
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It is also known that either CCl4 or SNS can affect systemic inflammatory responses. The aim of this study was to establish the effect of chemical sympathectomy with 6-hydroxydopamine (6-OHDA) in a mouse model of CCl4-induced acute hepatotoxicity and systemic inflammatory response. Mice exposed to CCl4 or vehicle were pretreated with 6-OHDA or saline. The serum levels of aminotransferases and alkaline phosphatase in the CCl4-poisoning mice with sympathetic denervation were significantly lower than those without sympathetic denervation. With sympathetic denervation, hepatocellular necrosis and fat infiltration induced by CCl4 were greatly decreased. Sympathetic denervation significantly attenuated CCl4-induced lipid peroxidation in liver and serum. Acute CCl4 intoxication showed increased expression of inflammatory cytokines/chemokines [eotaxin-2/CCL24, Fas ligand, interleukin (IL)-1α, IL-6, IL-12p40p70, monocyte chemoattractant protein-1 (MCP-1/CCL2), and tumor necrosis factor-α (TNF-α)], as well as decreased expression of granulocyte colony-stimulating factor and keratinocyte-derived chemokine. The overexpressed levels of IL-1α, IL-6, IL-12p40p70, MCP-1/CCL2, and TNF-α were attenuated by sympathetic denervation. Pretreatment with dexamethasone significantly reduced CCl4-induced hepatic injury. Collectively, this study demonstrates that the SNS plays an important role in CCl4-induced acute hepatotoxicity and systemic inflammation and the effect may be connected with chemical- or drug-induced hepatotoxicity and circulating immune response.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0121365</identifier><identifier>PMID: 25799095</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>6-Hydroxydopamine ; Alkaline phosphatase ; Alkaline Phosphatase - blood ; Analysis ; Animals ; Carbon tetrachloride ; Carbon Tetrachloride Poisoning - blood ; Carbon Tetrachloride Poisoning - complications ; Carbon Tetrachloride Poisoning - drug therapy ; Carbon Tetrachloride Poisoning - physiopathology ; CCL4 protein ; Chemokine CCL2 - blood ; Chemokines ; Chemokines - blood ; Colony-stimulating factor ; Cytokines ; Cytokines - blood ; Denervation ; Dexamethasone ; Dexamethasone - therapeutic use ; Drug dosages ; Eotaxin ; FasL protein ; Gastroenterology ; Gene expression ; Granulocyte colony-stimulating factor ; Hepatology ; Hepatotoxicity ; Hospitals ; Immune response ; Immune system ; Infiltration ; Inflammation ; Inflammatory response ; Injury prevention ; Interleukin 12 ; Interleukin 6 ; Internal medicine ; Intoxication ; Laboratory animals ; Leukocytes (granulocytic) ; Lipid peroxidation ; Liver ; Liver - pathology ; Male ; Medical research ; Medicine ; Metastases ; Mice ; Mice, Inbred C57BL ; Monocyte chemoattractant protein ; Monocyte chemoattractant protein 1 ; Nervous system ; Neurophysiology ; Pathogenesis ; Pathology ; Peroxidation ; Rodents ; Sympathetic nervous system ; Sympathetic Nervous System - physiopathology ; Systemic Inflammatory Response Syndrome - blood ; Systemic Inflammatory Response Syndrome - drug therapy ; Systemic Inflammatory Response Syndrome - etiology ; Systemic Inflammatory Response Syndrome - physiopathology ; Transaminases - blood</subject><ispartof>PloS one, 2015-03, Vol.10 (3), p.e0121365</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Lin et al 2015 Lin et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-47ed9f2a14718f51028b15c168d57112835651a5773af874437ad7917a783a443</citedby><cites>FETCH-LOGICAL-c692t-47ed9f2a14718f51028b15c168d57112835651a5773af874437ad7917a783a443</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/PMC4370606/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370606/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25799095$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ryffel, Bernhard</contributor><creatorcontrib>Lin, Jung-Chun</creatorcontrib><creatorcontrib>Peng, Yi-Jen</creatorcontrib><creatorcontrib>Wang, Shih-Yu</creatorcontrib><creatorcontrib>Young, Ton-Ho</creatorcontrib><creatorcontrib>Salter, Donald M</creatorcontrib><creatorcontrib>Lee, Herng-Sheng</creatorcontrib><title>Role of the sympathetic nervous system in carbon tetrachloride-induced hepatotoxicity and systemic inflammation</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Carbon tetrachloride (CCl4) is widely used as an animal model of hepatotoxicity and the mechanisms have been arduously studied, however, the contribution of the sympathetic nervous system (SNS) in CCl4-induced acute hepatotoxicity remains controversial. It is also known that either CCl4 or SNS can affect systemic inflammatory responses. The aim of this study was to establish the effect of chemical sympathectomy with 6-hydroxydopamine (6-OHDA) in a mouse model of CCl4-induced acute hepatotoxicity and systemic inflammatory response. Mice exposed to CCl4 or vehicle were pretreated with 6-OHDA or saline. The serum levels of aminotransferases and alkaline phosphatase in the CCl4-poisoning mice with sympathetic denervation were significantly lower than those without sympathetic denervation. With sympathetic denervation, hepatocellular necrosis and fat infiltration induced by CCl4 were greatly decreased. Sympathetic denervation significantly attenuated CCl4-induced lipid peroxidation in liver and serum. Acute CCl4 intoxication showed increased expression of inflammatory cytokines/chemokines [eotaxin-2/CCL24, Fas ligand, interleukin (IL)-1α, IL-6, IL-12p40p70, monocyte chemoattractant protein-1 (MCP-1/CCL2), and tumor necrosis factor-α (TNF-α)], as well as decreased expression of granulocyte colony-stimulating factor and keratinocyte-derived chemokine. The overexpressed levels of IL-1α, IL-6, IL-12p40p70, MCP-1/CCL2, and TNF-α were attenuated by sympathetic denervation. Pretreatment with dexamethasone significantly reduced CCl4-induced hepatic injury. Collectively, this study demonstrates that the SNS plays an important role in CCl4-induced acute hepatotoxicity and systemic inflammation and the effect may be connected with chemical- or drug-induced hepatotoxicity and circulating immune response.</description><subject>6-Hydroxydopamine</subject><subject>Alkaline phosphatase</subject><subject>Alkaline Phosphatase - blood</subject><subject>Analysis</subject><subject>Animals</subject><subject>Carbon tetrachloride</subject><subject>Carbon Tetrachloride Poisoning - blood</subject><subject>Carbon Tetrachloride Poisoning - complications</subject><subject>Carbon Tetrachloride Poisoning - drug therapy</subject><subject>Carbon Tetrachloride Poisoning - physiopathology</subject><subject>CCL4 protein</subject><subject>Chemokine CCL2 - blood</subject><subject>Chemokines</subject><subject>Chemokines - blood</subject><subject>Colony-stimulating factor</subject><subject>Cytokines</subject><subject>Cytokines - blood</subject><subject>Denervation</subject><subject>Dexamethasone</subject><subject>Dexamethasone - therapeutic use</subject><subject>Drug dosages</subject><subject>Eotaxin</subject><subject>FasL protein</subject><subject>Gastroenterology</subject><subject>Gene expression</subject><subject>Granulocyte colony-stimulating factor</subject><subject>Hepatology</subject><subject>Hepatotoxicity</subject><subject>Hospitals</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Infiltration</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Injury prevention</subject><subject>Interleukin 12</subject><subject>Interleukin 6</subject><subject>Internal medicine</subject><subject>Intoxication</subject><subject>Laboratory animals</subject><subject>Leukocytes (granulocytic)</subject><subject>Lipid peroxidation</subject><subject>Liver</subject><subject>Liver - pathology</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Monocyte chemoattractant protein</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Nervous system</subject><subject>Neurophysiology</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Peroxidation</subject><subject>Rodents</subject><subject>Sympathetic nervous system</subject><subject>Sympathetic Nervous System - physiopathology</subject><subject>Systemic Inflammatory Response Syndrome - blood</subject><subject>Systemic Inflammatory Response Syndrome - drug therapy</subject><subject>Systemic Inflammatory Response Syndrome - etiology</subject><subject>Systemic Inflammatory Response Syndrome - physiopathology</subject><subject>Transaminases - blood</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</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><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAYhYso7of-A9GCIHgxYz6apL1ZWBZXBxYW1o_b8E6aTjO0yZiky86_N3W6yxQUpBdN0uecvpycLHuD0RJTgT9t3eAtdMuds3qJMMGUs2fZKa4oWXCC6POj9Ul2FsIWIUZLzl9mJ4SJqkIVO83cnet07po8tjoP-34HaRGNyq32924I6SxE3efG5gr82tk86uhBtZ3zptYLY-tB6TpvdVK66B6MMnGfg60nZbIytumg7yEaZ19lLxrogn49vc-zH9efv199XdzcflldXd4sFK9IXBRC11VDABcClw3DiJRrzBTmZc0ExqSkjDMMTAgKTSmKggqoRYUFiJJC2p5n7w6-u84FOWUVJOY8GaKKskSsDkTtYCt33vTg99KBkX8OnN9I8CmJTkvChVqXGuMGVNEIUpW0EYyMwxCCuEheF9PfhnWva6Vtyqibmc6_WNPKjbuXaW7EEU8G7ycD734NOsR_jDxRG0hTpVjdeBW9CUpeFoSwosTVSC3_QqWnHm8jtaUx6Xwm-DgTJCbqh7iBIQS5-nb3_-ztzzn74YhtNXSxDa4bxh6EOVgcQOVdCF43T8lhJMeyP6Yhx7LLqexJ9vY49SfRY7vpb6WV-iw</recordid><startdate>20150323</startdate><enddate>20150323</enddate><creator>Lin, Jung-Chun</creator><creator>Peng, Yi-Jen</creator><creator>Wang, Shih-Yu</creator><creator>Young, Ton-Ho</creator><creator>Salter, Donald M</creator><creator>Lee, Herng-Sheng</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150323</creationdate><title>Role of the sympathetic nervous system in carbon tetrachloride-induced hepatotoxicity and systemic inflammation</title><author>Lin, Jung-Chun ; Peng, Yi-Jen ; Wang, Shih-Yu ; Young, Ton-Ho ; Salter, Donald M ; Lee, Herng-Sheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-47ed9f2a14718f51028b15c168d57112835651a5773af874437ad7917a783a443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>6-Hydroxydopamine</topic><topic>Alkaline phosphatase</topic><topic>Alkaline Phosphatase - blood</topic><topic>Analysis</topic><topic>Animals</topic><topic>Carbon tetrachloride</topic><topic>Carbon Tetrachloride Poisoning - blood</topic><topic>Carbon Tetrachloride Poisoning - complications</topic><topic>Carbon Tetrachloride Poisoning - drug therapy</topic><topic>Carbon Tetrachloride Poisoning - physiopathology</topic><topic>CCL4 protein</topic><topic>Chemokine CCL2 - blood</topic><topic>Chemokines</topic><topic>Chemokines - blood</topic><topic>Colony-stimulating factor</topic><topic>Cytokines</topic><topic>Cytokines - blood</topic><topic>Denervation</topic><topic>Dexamethasone</topic><topic>Dexamethasone - therapeutic use</topic><topic>Drug dosages</topic><topic>Eotaxin</topic><topic>FasL protein</topic><topic>Gastroenterology</topic><topic>Gene expression</topic><topic>Granulocyte colony-stimulating factor</topic><topic>Hepatology</topic><topic>Hepatotoxicity</topic><topic>Hospitals</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Infiltration</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Injury prevention</topic><topic>Interleukin 12</topic><topic>Interleukin 6</topic><topic>Internal medicine</topic><topic>Intoxication</topic><topic>Laboratory animals</topic><topic>Leukocytes (granulocytic)</topic><topic>Lipid peroxidation</topic><topic>Liver</topic><topic>Liver - pathology</topic><topic>Male</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Monocyte chemoattractant protein</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Nervous system</topic><topic>Neurophysiology</topic><topic>Pathogenesis</topic><topic>Pathology</topic><topic>Peroxidation</topic><topic>Rodents</topic><topic>Sympathetic nervous system</topic><topic>Sympathetic Nervous System - physiopathology</topic><topic>Systemic Inflammatory Response Syndrome - blood</topic><topic>Systemic Inflammatory Response Syndrome - drug therapy</topic><topic>Systemic Inflammatory Response Syndrome - etiology</topic><topic>Systemic Inflammatory Response Syndrome - physiopathology</topic><topic>Transaminases - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Jung-Chun</creatorcontrib><creatorcontrib>Peng, Yi-Jen</creatorcontrib><creatorcontrib>Wang, Shih-Yu</creatorcontrib><creatorcontrib>Young, Ton-Ho</creatorcontrib><creatorcontrib>Salter, Donald M</creatorcontrib><creatorcontrib>Lee, Herng-Sheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Jung-Chun</au><au>Peng, Yi-Jen</au><au>Wang, Shih-Yu</au><au>Young, Ton-Ho</au><au>Salter, Donald M</au><au>Lee, Herng-Sheng</au><au>Ryffel, Bernhard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of the sympathetic nervous system in carbon tetrachloride-induced hepatotoxicity and systemic inflammation</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-03-23</date><risdate>2015</risdate><volume>10</volume><issue>3</issue><spage>e0121365</spage><pages>e0121365-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Carbon tetrachloride (CCl4) is widely used as an animal model of hepatotoxicity and the mechanisms have been arduously studied, however, the contribution of the sympathetic nervous system (SNS) in CCl4-induced acute hepatotoxicity remains controversial. It is also known that either CCl4 or SNS can affect systemic inflammatory responses. The aim of this study was to establish the effect of chemical sympathectomy with 6-hydroxydopamine (6-OHDA) in a mouse model of CCl4-induced acute hepatotoxicity and systemic inflammatory response. Mice exposed to CCl4 or vehicle were pretreated with 6-OHDA or saline. The serum levels of aminotransferases and alkaline phosphatase in the CCl4-poisoning mice with sympathetic denervation were significantly lower than those without sympathetic denervation. With sympathetic denervation, hepatocellular necrosis and fat infiltration induced by CCl4 were greatly decreased. Sympathetic denervation significantly attenuated CCl4-induced lipid peroxidation in liver and serum. Acute CCl4 intoxication showed increased expression of inflammatory cytokines/chemokines [eotaxin-2/CCL24, Fas ligand, interleukin (IL)-1α, IL-6, IL-12p40p70, monocyte chemoattractant protein-1 (MCP-1/CCL2), and tumor necrosis factor-α (TNF-α)], as well as decreased expression of granulocyte colony-stimulating factor and keratinocyte-derived chemokine. The overexpressed levels of IL-1α, IL-6, IL-12p40p70, MCP-1/CCL2, and TNF-α were attenuated by sympathetic denervation. Pretreatment with dexamethasone significantly reduced CCl4-induced hepatic injury. Collectively, this study demonstrates that the SNS plays an important role in CCl4-induced acute hepatotoxicity and systemic inflammation and the effect may be connected with chemical- or drug-induced hepatotoxicity and circulating immune response.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25799095</pmid><doi>10.1371/journal.pone.0121365</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-03, Vol.10 (3), p.e0121365 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1667180935 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 6-Hydroxydopamine Alkaline phosphatase Alkaline Phosphatase - blood Analysis Animals Carbon tetrachloride Carbon Tetrachloride Poisoning - blood Carbon Tetrachloride Poisoning - complications Carbon Tetrachloride Poisoning - drug therapy Carbon Tetrachloride Poisoning - physiopathology CCL4 protein Chemokine CCL2 - blood Chemokines Chemokines - blood Colony-stimulating factor Cytokines Cytokines - blood Denervation Dexamethasone Dexamethasone - therapeutic use Drug dosages Eotaxin FasL protein Gastroenterology Gene expression Granulocyte colony-stimulating factor Hepatology Hepatotoxicity Hospitals Immune response Immune system Infiltration Inflammation Inflammatory response Injury prevention Interleukin 12 Interleukin 6 Internal medicine Intoxication Laboratory animals Leukocytes (granulocytic) Lipid peroxidation Liver Liver - pathology Male Medical research Medicine Metastases Mice Mice, Inbred C57BL Monocyte chemoattractant protein Monocyte chemoattractant protein 1 Nervous system Neurophysiology Pathogenesis Pathology Peroxidation Rodents Sympathetic nervous system Sympathetic Nervous System - physiopathology Systemic Inflammatory Response Syndrome - blood Systemic Inflammatory Response Syndrome - drug therapy Systemic Inflammatory Response Syndrome - etiology Systemic Inflammatory Response Syndrome - physiopathology Transaminases - blood |
| title | Role of the sympathetic nervous system in carbon tetrachloride-induced hepatotoxicity and systemic inflammation |
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