Acetaminophen-induced liver injury alters the Acyl ethanolamine-based anti-inflammatory signaling system in liver

Protective mechanisms against drug-induced liver injury are actively being searched to identify new therapeutic targets. Among them, the anti-inflammatory N-acyl ethanolamide (NAE)-peroxisome proliferators activated receptor alpha (PPARα) system has gained much interest after the identification of i...

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Autores: Rivera, Patricia, Pastor, Antonio, Arrabal, Sergio, Decara, Juan M., Vargas, Antonio, Sánchez-Marín, Laura, Pavón, Francisco Javier, Serrano, Antonia, Bautista, Dolores, Boronat Rigol, Anna, 1990-, Torre Fornell, Rafael de la, Baixeras, Elena, Lucena, Maria Isabel, Rodríguez de Fonseca, Fernando, Suárez, Juan
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2017
País:España
Institución:Universitat Pompeu Fabra
Repositorio:Repositorio Digital de la UPF
OAI Identifier:oai:repositori.upf.edu:10230/34066
Acceso en línea:http://hdl.handle.net/10230/34066
http://dx.doi.org/10.3389/fphar.2017.00705
Access Level:acceso abierto
Palabra clave:FAAH
OEA
PPARα
Hepatic injury
Paracetamol
Toxicity
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spelling Acetaminophen-induced liver injury alters the Acyl ethanolamine-based anti-inflammatory signaling system in liverRivera, PatriciaPastor, AntonioArrabal, SergioDecara, Juan M.Vargas, AntonioSánchez-Marín, LauraPavón, Francisco JavierSerrano, AntoniaBautista, DoloresBoronat Rigol, Anna, 1990-Torre Fornell, Rafael de laBaixeras, ElenaLucena, Maria IsabelRodríguez de Fonseca, FernandoSuárez, JuanFAAHOEAPPARαHepatic injuryParacetamolToxicityProtective mechanisms against drug-induced liver injury are actively being searched to identify new therapeutic targets. Among them, the anti-inflammatory N-acyl ethanolamide (NAE)-peroxisome proliferators activated receptor alpha (PPARα) system has gained much interest after the identification of its protective role in steatohepatitis and liver fibrosis. An overdose of paracetamol (APAP), a commonly used analgesic/antipyretic drug, causes hepatotoxicity, and it is being used as a liver model. In the present study, we have analyzed the impact of APAP on the liver NAE-PPARα system. A dose-response (0.5-5-10-20 mM) and time-course (2-6-24 h) study in human HepG2 cells showed a biphasic response, with a decreased PPARα expression after 6-h APAP incubation followed by a generalized increase of NAE-PPARα system-related components (PPARα, NAPE-PLD, and FAAH), including the NAEs oleoyl ethanolamide (OEA) and docosahexaenoyl ethanolamide, after a 24-h exposure to APAP. These results were partially confirmed in a time-course study of mice exposed to an acute dose of APAP (750 mg/kg). The gene expression levels of Pparα and Faah were decreased after 6 h of treatment and, after 24 h, the gene expression levels of Nape-pld and Faah, as well as the liver levels of OEA and palmitoyl ethanolamide, were increased. Repeated APAP administration (750 mg/kg/day) up to 4 days also decreased the expression levels of PPARα and FAAH, and increased the liver levels of NAEs. A resting period of 15 days completely restored these impairments. Liver immunohistochemistry in a well-characterized human case of APAP hepatotoxicity confirmed PPARα and FAAH decrements. Histopathological and hepatic damage (Cyp2e1, Caspase3, αSma, Tnfα, and Mcp1)-related alterations observed after repeated APAP administration were aggravated in the liver of Pparα-deficient mice. Our results demonstrate that the anti-inflammatory NAE-PPARα signaling system is implicated in liver toxicity after exposure to APAP overdose, and may contribute to its recovery through a long-term time-dependent response.Frontiers201820182017info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttp://hdl.handle.net/10230/34066http://dx.doi.org/10.3389/fphar.2017.00705reponame:Repositorio Digital de la UPFinstname:Universitat Pompeu FabraInglésFront Pharmacol. 2017 Oct 6;8:705© 2017 Rivera, Pastor, Arrabal, Decara, Vargas, Sánchez-Marín, Pavón, Serrano, Bautista, Boronat, de la Torre, Baixeras, Lucena, de Fonseca and Suárez. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) (http://creativecommons.org/licenses/by/4.0/). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.http://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:repositori.upf.edu:10230/340662026-06-12T07:21:37Z
dc.title.none.fl_str_mv Acetaminophen-induced liver injury alters the Acyl ethanolamine-based anti-inflammatory signaling system in liver
title Acetaminophen-induced liver injury alters the Acyl ethanolamine-based anti-inflammatory signaling system in liver
spellingShingle Acetaminophen-induced liver injury alters the Acyl ethanolamine-based anti-inflammatory signaling system in liver
Rivera, Patricia
FAAH
OEA
PPARα
Hepatic injury
Paracetamol
Toxicity
title_short Acetaminophen-induced liver injury alters the Acyl ethanolamine-based anti-inflammatory signaling system in liver
title_full Acetaminophen-induced liver injury alters the Acyl ethanolamine-based anti-inflammatory signaling system in liver
title_fullStr Acetaminophen-induced liver injury alters the Acyl ethanolamine-based anti-inflammatory signaling system in liver
title_full_unstemmed Acetaminophen-induced liver injury alters the Acyl ethanolamine-based anti-inflammatory signaling system in liver
title_sort Acetaminophen-induced liver injury alters the Acyl ethanolamine-based anti-inflammatory signaling system in liver
dc.creator.none.fl_str_mv Rivera, Patricia
Pastor, Antonio
Arrabal, Sergio
Decara, Juan M.
Vargas, Antonio
Sánchez-Marín, Laura
Pavón, Francisco Javier
Serrano, Antonia
Bautista, Dolores
Boronat Rigol, Anna, 1990-
Torre Fornell, Rafael de la
Baixeras, Elena
Lucena, Maria Isabel
Rodríguez de Fonseca, Fernando
Suárez, Juan
author Rivera, Patricia
author_facet Rivera, Patricia
Pastor, Antonio
Arrabal, Sergio
Decara, Juan M.
Vargas, Antonio
Sánchez-Marín, Laura
Pavón, Francisco Javier
Serrano, Antonia
Bautista, Dolores
Boronat Rigol, Anna, 1990-
Torre Fornell, Rafael de la
Baixeras, Elena
Lucena, Maria Isabel
Rodríguez de Fonseca, Fernando
Suárez, Juan
author_role author
author2 Pastor, Antonio
Arrabal, Sergio
Decara, Juan M.
Vargas, Antonio
Sánchez-Marín, Laura
Pavón, Francisco Javier
Serrano, Antonia
Bautista, Dolores
Boronat Rigol, Anna, 1990-
Torre Fornell, Rafael de la
Baixeras, Elena
Lucena, Maria Isabel
Rodríguez de Fonseca, Fernando
Suárez, Juan
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv FAAH
OEA
PPARα
Hepatic injury
Paracetamol
Toxicity
topic FAAH
OEA
PPARα
Hepatic injury
Paracetamol
Toxicity
description Protective mechanisms against drug-induced liver injury are actively being searched to identify new therapeutic targets. Among them, the anti-inflammatory N-acyl ethanolamide (NAE)-peroxisome proliferators activated receptor alpha (PPARα) system has gained much interest after the identification of its protective role in steatohepatitis and liver fibrosis. An overdose of paracetamol (APAP), a commonly used analgesic/antipyretic drug, causes hepatotoxicity, and it is being used as a liver model. In the present study, we have analyzed the impact of APAP on the liver NAE-PPARα system. A dose-response (0.5-5-10-20 mM) and time-course (2-6-24 h) study in human HepG2 cells showed a biphasic response, with a decreased PPARα expression after 6-h APAP incubation followed by a generalized increase of NAE-PPARα system-related components (PPARα, NAPE-PLD, and FAAH), including the NAEs oleoyl ethanolamide (OEA) and docosahexaenoyl ethanolamide, after a 24-h exposure to APAP. These results were partially confirmed in a time-course study of mice exposed to an acute dose of APAP (750 mg/kg). The gene expression levels of Pparα and Faah were decreased after 6 h of treatment and, after 24 h, the gene expression levels of Nape-pld and Faah, as well as the liver levels of OEA and palmitoyl ethanolamide, were increased. Repeated APAP administration (750 mg/kg/day) up to 4 days also decreased the expression levels of PPARα and FAAH, and increased the liver levels of NAEs. A resting period of 15 days completely restored these impairments. Liver immunohistochemistry in a well-characterized human case of APAP hepatotoxicity confirmed PPARα and FAAH decrements. Histopathological and hepatic damage (Cyp2e1, Caspase3, αSma, Tnfα, and Mcp1)-related alterations observed after repeated APAP administration were aggravated in the liver of Pparα-deficient mice. Our results demonstrate that the anti-inflammatory NAE-PPARα signaling system is implicated in liver toxicity after exposure to APAP overdose, and may contribute to its recovery through a long-term time-dependent response.
publishDate 2017
dc.date.none.fl_str_mv 2017
2018
2018
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10230/34066
http://dx.doi.org/10.3389/fphar.2017.00705
url http://hdl.handle.net/10230/34066
http://dx.doi.org/10.3389/fphar.2017.00705
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Front Pharmacol. 2017 Oct 6;8:705
dc.rights.none.fl_str_mv http://creativecommons.org/licenses/by/4.0/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Frontiers
publisher.none.fl_str_mv Frontiers
dc.source.none.fl_str_mv reponame:Repositorio Digital de la UPF
instname:Universitat Pompeu Fabra
instname_str Universitat Pompeu Fabra
reponame_str Repositorio Digital de la UPF
collection Repositorio Digital de la UPF
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