The role of annexin A1-derived peptide Ac2–26 on liver and kidney injuries induced by cisplatin in rats
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1016/j.lfs.2022.120677 http://hdl.handle.net/11449/240336 |
Resumo: | Aims: In this study we evaluated the effect of pharmacological treatment with AnxA1-derived peptide Ac2–26 in an experimental model of toxicity induced by cisplatin. Main methods: Male rats were divided into Sham (control), Cisplatin (received intraperitoneal injections of 10 mg/kg/day of cisplatin for 3 days) and Ac2–26 (received intraperitoneal injections of 1 mg/kg/day of peptide, 15 min before cisplatin) groups. Key findings: After 6 h of the last dose of cisplatin, an acute inflammatory response was observed characterized by a marked increase in the number of neutrophils and GM-CSF, IL-β, IL-6, IL-10 and TNF-α plasma levels. These findings were associated with increased AnxA1 protein levels in liver and kidneys, as well as positive AnxA1/Fpr2 circulating leukocytes. Treatment with Ac2–26 produced higher levels of GM-CSF, corroborating the high numbers of neutrophils, and the anti-inflammatory cytokine IL-4. Ac2–26 preserved the morphology of liver structures and increased Fpr1 expression, preventing the damage caused by cisplatin. In the kidneys, Ac2–26 caused downregulation of renal Fpr1 and Fpr2 levels and abrogated the increased levels of the CLU and KIM-1 biomarkers of kidney damage induced by cisplatin. However, no effect of peptide treatment was detected in cisplatin-induced kidney morphology injury. Significance: Despite activation of the anti-inflammatory AnxA1/Fpr axis during cisplatin administration, treatment with Ac2–26 did not efficiently prevent its deleterious effects on the liver and kidneys. |
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The role of annexin A1-derived peptide Ac2–26 on liver and kidney injuries induced by cisplatin in ratsFormyl peptide receptorsHepatotoxicityInflammationNephrotoxicityNeutrophilAims: In this study we evaluated the effect of pharmacological treatment with AnxA1-derived peptide Ac2–26 in an experimental model of toxicity induced by cisplatin. Main methods: Male rats were divided into Sham (control), Cisplatin (received intraperitoneal injections of 10 mg/kg/day of cisplatin for 3 days) and Ac2–26 (received intraperitoneal injections of 1 mg/kg/day of peptide, 15 min before cisplatin) groups. Key findings: After 6 h of the last dose of cisplatin, an acute inflammatory response was observed characterized by a marked increase in the number of neutrophils and GM-CSF, IL-β, IL-6, IL-10 and TNF-α plasma levels. These findings were associated with increased AnxA1 protein levels in liver and kidneys, as well as positive AnxA1/Fpr2 circulating leukocytes. Treatment with Ac2–26 produced higher levels of GM-CSF, corroborating the high numbers of neutrophils, and the anti-inflammatory cytokine IL-4. Ac2–26 preserved the morphology of liver structures and increased Fpr1 expression, preventing the damage caused by cisplatin. In the kidneys, Ac2–26 caused downregulation of renal Fpr1 and Fpr2 levels and abrogated the increased levels of the CLU and KIM-1 biomarkers of kidney damage induced by cisplatin. However, no effect of peptide treatment was detected in cisplatin-induced kidney morphology injury. Significance: Despite activation of the anti-inflammatory AnxA1/Fpr axis during cisplatin administration, treatment with Ac2–26 did not efficiently prevent its deleterious effects on the liver and kidneys.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Department of Morphology and Genetics Universidade Federal de São Paulo (UNIFESP), SPDepartment of Medicine Nephology Division Universidade Federal de São Paulo (UNIFESP), SPBiosciences Graduate Program Institute of Biosciences Letters and Exact Sciences Universidade Estadual Paulista (UNESP), SPAdvanced Research Center in Medicine (CEPAM) Unilago, SPBiosciences Graduate Program Institute of Biosciences Letters and Exact Sciences Universidade Estadual Paulista (UNESP), SPFAPESP: 19/14331-5Universidade Federal de São Paulo (UNIFESP)Universidade Estadual Paulista (UNESP)Advanced Research Center in Medicine (CEPAM) UnilagoLucchi, Danilo B.M.Sasso, Gisela R.S.Sena, Letícia S.Santos, Diego D. [UNESP]Franco, Paulo C.Lice, IzabellaBorges, Fernanda T.Oliani, Sonia M. [UNESP]Gil, Cristiane D. [UNESP]2023-03-01T20:12:32Z2023-03-01T20:12:32Z2022-09-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1016/j.lfs.2022.120677Life Sciences, v. 304.1879-06310024-3205http://hdl.handle.net/11449/24033610.1016/j.lfs.2022.1206772-s2.0-85132766977Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengLife Sciencesinfo:eu-repo/semantics/openAccess2023-03-01T20:12:32Zoai:repositorio.unesp.br:11449/240336Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T18:12:58.623543Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
The role of annexin A1-derived peptide Ac2–26 on liver and kidney injuries induced by cisplatin in rats |
title |
The role of annexin A1-derived peptide Ac2–26 on liver and kidney injuries induced by cisplatin in rats |
spellingShingle |
The role of annexin A1-derived peptide Ac2–26 on liver and kidney injuries induced by cisplatin in rats Lucchi, Danilo B.M. Formyl peptide receptors Hepatotoxicity Inflammation Nephrotoxicity Neutrophil |
title_short |
The role of annexin A1-derived peptide Ac2–26 on liver and kidney injuries induced by cisplatin in rats |
title_full |
The role of annexin A1-derived peptide Ac2–26 on liver and kidney injuries induced by cisplatin in rats |
title_fullStr |
The role of annexin A1-derived peptide Ac2–26 on liver and kidney injuries induced by cisplatin in rats |
title_full_unstemmed |
The role of annexin A1-derived peptide Ac2–26 on liver and kidney injuries induced by cisplatin in rats |
title_sort |
The role of annexin A1-derived peptide Ac2–26 on liver and kidney injuries induced by cisplatin in rats |
author |
Lucchi, Danilo B.M. |
author_facet |
Lucchi, Danilo B.M. Sasso, Gisela R.S. Sena, Letícia S. Santos, Diego D. [UNESP] Franco, Paulo C. Lice, Izabella Borges, Fernanda T. Oliani, Sonia M. [UNESP] Gil, Cristiane D. [UNESP] |
author_role |
author |
author2 |
Sasso, Gisela R.S. Sena, Letícia S. Santos, Diego D. [UNESP] Franco, Paulo C. Lice, Izabella Borges, Fernanda T. Oliani, Sonia M. [UNESP] Gil, Cristiane D. [UNESP] |
author2_role |
author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) Universidade Estadual Paulista (UNESP) Advanced Research Center in Medicine (CEPAM) Unilago |
dc.contributor.author.fl_str_mv |
Lucchi, Danilo B.M. Sasso, Gisela R.S. Sena, Letícia S. Santos, Diego D. [UNESP] Franco, Paulo C. Lice, Izabella Borges, Fernanda T. Oliani, Sonia M. [UNESP] Gil, Cristiane D. [UNESP] |
dc.subject.por.fl_str_mv |
Formyl peptide receptors Hepatotoxicity Inflammation Nephrotoxicity Neutrophil |
topic |
Formyl peptide receptors Hepatotoxicity Inflammation Nephrotoxicity Neutrophil |
description |
Aims: In this study we evaluated the effect of pharmacological treatment with AnxA1-derived peptide Ac2–26 in an experimental model of toxicity induced by cisplatin. Main methods: Male rats were divided into Sham (control), Cisplatin (received intraperitoneal injections of 10 mg/kg/day of cisplatin for 3 days) and Ac2–26 (received intraperitoneal injections of 1 mg/kg/day of peptide, 15 min before cisplatin) groups. Key findings: After 6 h of the last dose of cisplatin, an acute inflammatory response was observed characterized by a marked increase in the number of neutrophils and GM-CSF, IL-β, IL-6, IL-10 and TNF-α plasma levels. These findings were associated with increased AnxA1 protein levels in liver and kidneys, as well as positive AnxA1/Fpr2 circulating leukocytes. Treatment with Ac2–26 produced higher levels of GM-CSF, corroborating the high numbers of neutrophils, and the anti-inflammatory cytokine IL-4. Ac2–26 preserved the morphology of liver structures and increased Fpr1 expression, preventing the damage caused by cisplatin. In the kidneys, Ac2–26 caused downregulation of renal Fpr1 and Fpr2 levels and abrogated the increased levels of the CLU and KIM-1 biomarkers of kidney damage induced by cisplatin. However, no effect of peptide treatment was detected in cisplatin-induced kidney morphology injury. Significance: Despite activation of the anti-inflammatory AnxA1/Fpr axis during cisplatin administration, treatment with Ac2–26 did not efficiently prevent its deleterious effects on the liver and kidneys. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-09-01 2023-03-01T20:12:32Z 2023-03-01T20:12:32Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1016/j.lfs.2022.120677 Life Sciences, v. 304. 1879-0631 0024-3205 http://hdl.handle.net/11449/240336 10.1016/j.lfs.2022.120677 2-s2.0-85132766977 |
url |
http://dx.doi.org/10.1016/j.lfs.2022.120677 http://hdl.handle.net/11449/240336 |
identifier_str_mv |
Life Sciences, v. 304. 1879-0631 0024-3205 10.1016/j.lfs.2022.120677 2-s2.0-85132766977 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Life Sciences |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
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1808128908134973440 |