Proliferative Activity in Ischemia/Reperfusion Injury in Hepatectomized Mice: Effect of N-Acetylcysteine
Autor(a) principal: | |
---|---|
Data de Publicação: | 2012 |
Outros Autores: | , , , |
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. |
id |
UFSP_df293a75ce2aac354700430aaec33b43 |
---|---|
oai_identifier_str |
oai:repositorio.unifesp.br/:11600/35305 |
network_acronym_str |
UFSP |
network_name_str |
Repositório Institucional da UNIFESP |
repository_id_str |
3465 |
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 |
_version_ |
1814268437126447104 |