Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-Acetylcysteine

Detalhes bibliográficos
Autor(a) principal: Silva, S. M.
Data de Publicação: 2012
Outros Autores: Carbonel, Adriana Aparecida Ferraz [UNIFESP], Taha, Murched Omar [UNIFESP], Simoes, M. J., Montero, Edna Frasson de Souza [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://dx.doi.org/10.1016/j.transproceed.2012.07.009
http://repositorio.unifesp.br/handle/11600/35305
Resumo: Background. Dysfunction of the liver after transplantation may be related to the graft size and ischemia/reperfusion (I/R) injury. N-Acetylcysteine (NAC) exerts beneficial effects on livers undergoing ischemia reperfusion. We sought to evaluate NAC modulation on reduced livers associated with I/R injury.Methods. Male C57BL/6 mice of 8 weeks of age were divided into groups: 50% hepatectomy (G-Hep); NAC (G-Hep + NAC [150 mg/kg]) via vena cava 15 minutes before hepatectomy; ischemia (G-Hep + IR); NAC with hepatectomy (G-IR + Hep + Nac); and IR using 30 minutes selective hepatic occlusion and reperfusion for 24 hours. After 24 hours, the remaining liver was removed, for staining with hematoxylin and eosin or labeling by proliferating cell nuclear antigen. Blood was collected for biochemical evaluations. Significance was considered for P <= .05.Results. Aspartate aminotransferase was high in all studied groups reflecting the hepatectomy and intervention. injuries. However, when assessing alanine aminotransferase, which depicts liver function, induction of IR promoted a greater increase than hepatectomy (P = .0003). NAC decreased ALT activity in all groups, even in association with I/R (P < .05), reflecting a modulation of the injury. Necrosis resulting from IR was mitigated by NAC. the experimental model of 50% reduced live promoted regeneration of the hepatic remnant, which was accentuated by NAC, according to the total number of hepatocytes and PCNA values.Conclusion. NAC preserved the remnant liver in mice and stimulates regeneration even after IR injury.
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spelling Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-AcetylcysteineBackground. Dysfunction of the liver after transplantation may be related to the graft size and ischemia/reperfusion (I/R) injury. N-Acetylcysteine (NAC) exerts beneficial effects on livers undergoing ischemia reperfusion. We sought to evaluate NAC modulation on reduced livers associated with I/R injury.Methods. Male C57BL/6 mice of 8 weeks of age were divided into groups: 50% hepatectomy (G-Hep); NAC (G-Hep + NAC [150 mg/kg]) via vena cava 15 minutes before hepatectomy; ischemia (G-Hep + IR); NAC with hepatectomy (G-IR + Hep + Nac); and IR using 30 minutes selective hepatic occlusion and reperfusion for 24 hours. After 24 hours, the remaining liver was removed, for staining with hematoxylin and eosin or labeling by proliferating cell nuclear antigen. Blood was collected for biochemical evaluations. Significance was considered for P <= .05.Results. Aspartate aminotransferase was high in all studied groups reflecting the hepatectomy and intervention. injuries. However, when assessing alanine aminotransferase, which depicts liver function, induction of IR promoted a greater increase than hepatectomy (P = .0003). NAC decreased ALT activity in all groups, even in association with I/R (P < .05), reflecting a modulation of the injury. Necrosis resulting from IR was mitigated by NAC. the experimental model of 50% reduced live promoted regeneration of the hepatic remnant, which was accentuated by NAC, according to the total number of hepatocytes and PCNA values.Conclusion. NAC preserved the remnant liver in mice and stimulates regeneration even after IR injury.Univ São Paulo, Dept Sci, São Paulo, BrazilUniv São Paulo, Dept Gynecol & Genet, São Paulo, BrazilUniv São Paulo, Dept Histol, São Paulo, BrazilUniv São Paulo, Dept Surg, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Surg, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Surg, São Paulo, BrazilWeb of ScienceElsevier B.V.Universidade de São Paulo (USP)Universidade Federal de São Paulo (UNIFESP)Silva, S. M.Carbonel, Adriana Aparecida Ferraz [UNIFESP]Taha, Murched Omar [UNIFESP]Simoes, M. J.Montero, Edna Frasson de Souza [UNIFESP]2016-01-24T14:27:44Z2016-01-24T14:27:44Z2012-10-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion2321-2325application/pdfhttp://dx.doi.org/10.1016/j.transproceed.2012.07.009Transplantation Proceedings. New York: Elsevier B.V., v. 44, n. 8, p. 2321-2325, 2012.10.1016/j.transproceed.2012.07.009WOS000309736900017.pdf0041-1345http://repositorio.unifesp.br/handle/11600/35305WOS:000309736900017engTransplantation Proceedingsinfo:eu-repo/semantics/openAccesshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policyreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-08-08T15:06:49Zoai:repositorio.unifesp.br/:11600/35305Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-08-08T15:06:49Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-Acetylcysteine
title Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-Acetylcysteine
spellingShingle Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-Acetylcysteine
Silva, S. M.
title_short Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-Acetylcysteine
title_full Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-Acetylcysteine
title_fullStr Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-Acetylcysteine
title_full_unstemmed Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-Acetylcysteine
title_sort Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-Acetylcysteine
author Silva, S. M.
author_facet Silva, S. M.
Carbonel, Adriana Aparecida Ferraz [UNIFESP]
Taha, Murched Omar [UNIFESP]
Simoes, M. J.
Montero, Edna Frasson de Souza [UNIFESP]
author_role author
author2 Carbonel, Adriana Aparecida Ferraz [UNIFESP]
Taha, Murched Omar [UNIFESP]
Simoes, M. J.
Montero, Edna Frasson de Souza [UNIFESP]
author2_role author
author
author
author
dc.contributor.none.fl_str_mv Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
dc.contributor.author.fl_str_mv Silva, S. M.
Carbonel, Adriana Aparecida Ferraz [UNIFESP]
Taha, Murched Omar [UNIFESP]
Simoes, M. J.
Montero, Edna Frasson de Souza [UNIFESP]
description Background. Dysfunction of the liver after transplantation may be related to the graft size and ischemia/reperfusion (I/R) injury. N-Acetylcysteine (NAC) exerts beneficial effects on livers undergoing ischemia reperfusion. We sought to evaluate NAC modulation on reduced livers associated with I/R injury.Methods. Male C57BL/6 mice of 8 weeks of age were divided into groups: 50% hepatectomy (G-Hep); NAC (G-Hep + NAC [150 mg/kg]) via vena cava 15 minutes before hepatectomy; ischemia (G-Hep + IR); NAC with hepatectomy (G-IR + Hep + Nac); and IR using 30 minutes selective hepatic occlusion and reperfusion for 24 hours. After 24 hours, the remaining liver was removed, for staining with hematoxylin and eosin or labeling by proliferating cell nuclear antigen. Blood was collected for biochemical evaluations. Significance was considered for P <= .05.Results. Aspartate aminotransferase was high in all studied groups reflecting the hepatectomy and intervention. injuries. However, when assessing alanine aminotransferase, which depicts liver function, induction of IR promoted a greater increase than hepatectomy (P = .0003). NAC decreased ALT activity in all groups, even in association with I/R (P < .05), reflecting a modulation of the injury. Necrosis resulting from IR was mitigated by NAC. the experimental model of 50% reduced live promoted regeneration of the hepatic remnant, which was accentuated by NAC, according to the total number of hepatocytes and PCNA values.Conclusion. NAC preserved the remnant liver in mice and stimulates regeneration even after IR injury.
publishDate 2012
dc.date.none.fl_str_mv 2012-10-01
2016-01-24T14:27:44Z
2016-01-24T14:27:44Z
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1016/j.transproceed.2012.07.009
Transplantation Proceedings. New York: Elsevier B.V., v. 44, n. 8, p. 2321-2325, 2012.
10.1016/j.transproceed.2012.07.009
WOS000309736900017.pdf
0041-1345
http://repositorio.unifesp.br/handle/11600/35305
WOS:000309736900017
url http://dx.doi.org/10.1016/j.transproceed.2012.07.009
http://repositorio.unifesp.br/handle/11600/35305
identifier_str_mv Transplantation Proceedings. New York: Elsevier B.V., v. 44, n. 8, p. 2321-2325, 2012.
10.1016/j.transproceed.2012.07.009
WOS000309736900017.pdf
0041-1345
WOS:000309736900017
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Transplantation Proceedings
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
eu_rights_str_mv openAccess
rights_invalid_str_mv http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.format.none.fl_str_mv 2321-2325
application/pdf
dc.publisher.none.fl_str_mv Elsevier B.V.
publisher.none.fl_str_mv Elsevier B.V.
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv biblioteca.csp@unifesp.br
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