Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos

Detalhes bibliográficos
Ano de defesa: 2013
Autor(a) principal: Lima, Patricia Rodrigues
Orientador(a): Santos, Flávia Almeida
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Não Informado pela instituição
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://www.repositorio.ufc.br/handle/riufc/11957
Resumo: Acute pancreatitis (AP) is an inflammatory condition in which pro-inflammatory mediators, oxidative stress and NF-kB signaling have a fundamental role. The 1,8-cineole, a monoterpene present in several plants species, is known for its antioxidant and anti-inflammatory potential. In order to verify its efficacy preventing AP, this study evaluated 1,8-cineole (100, 200 and 400 mg/kg, oral) on AP induced by cerulein (50 µg / kg / h × 5, i.p.) in Swiss mice. The 1,8-cineole was administrated one hour before the first injection of cerulein. Groups treated with vehicle or thalidomide were included as controls. Six hours later, blood samples were collected to determine blood levels of amylase, lipase and cytokines. The pancreas was removed for morphological examination, myeloperoxidase (MPO) and malondialdehyde (MDA) trials, changes in reduced glutathione (GSH) and for immunostaining of nuclear factor NF-κB. The right lung was removed for MPO trial. The 1,8-cineole reduced the histological damage and the expression of NF-κB induced by cerulein. Cerulein increased significantly amylase, lipase, TNF- α, IL1- β and IL-6, reducing IL-10. The 1,8-cineole 100, 200 and 400 mg/kg reversed significantly the damages caused by cerulein by reducing amylase (14; 16; 21 %), lipase (49; 48; 42 %), TNF-α (46; 66; 44 %), IL1-β (53; 45 e 67 %) e IL-6 (49; 40; 41 %) and enhanced IL-10 (34; 29 e 46 %), respectively. Cerulein produced pancreatic edema, increased MDA, pancreatic MPO, pulmonary MPO and decreased GSH comparing to the vehicle group (p < 0,05). The 1,8 cineole 100, 200 and 400 mg/kg reduced pancreatic edema (6; 27; 17%), MDA (34; 29; 46%), pancreatic MPO (40; 55 and 78 %), pulmonary MPO (42; 45 and 22 %) and preserved GSH (62; 63 and 65 %). These findings suggest that 1,8-cineol can prevent the severity of cerulein-induced acute pancreatitis in mice through an anti-inflammatory and antioxidant mechanisms.
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spelling Lima, Patricia RodriguesRao, Vietla SatyanarayanaSantos, Flávia Almeida2015-05-11T13:14:13Z2015-05-11T13:14:13Z2013LIMA, Patricia Rodrigues. Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos. Dissertação (Mestrado em Ciências Médicas) - Faculdade de Medicina, Universidade Federal do Ceará, Fortaleza, 2013.http://www.repositorio.ufc.br/handle/riufc/11957Acute pancreatitis (AP) is an inflammatory condition in which pro-inflammatory mediators, oxidative stress and NF-kB signaling have a fundamental role. The 1,8-cineole, a monoterpene present in several plants species, is known for its antioxidant and anti-inflammatory potential. In order to verify its efficacy preventing AP, this study evaluated 1,8-cineole (100, 200 and 400 mg/kg, oral) on AP induced by cerulein (50 µg / kg / h × 5, i.p.) in Swiss mice. The 1,8-cineole was administrated one hour before the first injection of cerulein. Groups treated with vehicle or thalidomide were included as controls. Six hours later, blood samples were collected to determine blood levels of amylase, lipase and cytokines. The pancreas was removed for morphological examination, myeloperoxidase (MPO) and malondialdehyde (MDA) trials, changes in reduced glutathione (GSH) and for immunostaining of nuclear factor NF-κB. The right lung was removed for MPO trial. The 1,8-cineole reduced the histological damage and the expression of NF-κB induced by cerulein. Cerulein increased significantly amylase, lipase, TNF- α, IL1- β and IL-6, reducing IL-10. The 1,8-cineole 100, 200 and 400 mg/kg reversed significantly the damages caused by cerulein by reducing amylase (14; 16; 21 %), lipase (49; 48; 42 %), TNF-α (46; 66; 44 %), IL1-β (53; 45 e 67 %) e IL-6 (49; 40; 41 %) and enhanced IL-10 (34; 29 e 46 %), respectively. Cerulein produced pancreatic edema, increased MDA, pancreatic MPO, pulmonary MPO and decreased GSH comparing to the vehicle group (p < 0,05). The 1,8 cineole 100, 200 and 400 mg/kg reduced pancreatic edema (6; 27; 17%), MDA (34; 29; 46%), pancreatic MPO (40; 55 and 78 %), pulmonary MPO (42; 45 and 22 %) and preserved GSH (62; 63 and 65 %). These findings suggest that 1,8-cineol can prevent the severity of cerulein-induced acute pancreatitis in mice through an anti-inflammatory and antioxidant mechanisms.Pancreatite aguda (PA) é uma doença inflamatória em que mediadores pró-inflamatórios, estresse oxidativo e sinalização de NF- kB desempenham um papel fundamental. O 1,8-cineol, um monoterpeno presente em diversas espécies vegetais, é conhecido por seu potencial antioxidante e anti-inflamatório. Para verificar a sua eficácia na prevenção da PA, este estudo avaliou o 1,8-cineol (100, 200 e 400 mg / kg, v.o) na PA induzida por ceruleína (50 µg / kg / h × 5, i.p.) em camundongos Swiss. O 1,8-cineol foi administrado uma hora antes da primeira injeção de ceruleína. Grupos tratados com veículo ou talidomida foram incluídos como controles. Seis horas depois, as amostras de sangue foram coletadas para determinar os níveis séricos de amilase, lipase e citocinas. O pâncreas foi removido para exame morfológico, ensaios de mieloperoxidase (MPO) e malondialdeído (MDA), alterações na glutationa reduzida (GSH) e para a imunocoloração do fator nuclear NF-κB. O pulmão direito foi removido para ensaio de MPO. O 1,8-cineol reduziu o dano histológico e a expressão de NF-κB induzidos por ceruleína. Ceruleína aumentou significativamente a amilase, lipase, TNF-α, IL1-β e IL-6 e reduziu IL-10. O 1,8-cineol 100, 200 e 400 mg/kg reverteu significativamente os danos causados pela ceruleína, através da redução da amilase (14; 16; 21%), lipase (49; 48; 42%), TNF-α (46; 66; 44%), IL1-β (53; 45 e 67%) e IL-6 (49; 40; 41%) e aumento da IL-10 (34; 29 e 46%), respectivamente. Ceruleína produziu edema pancreático, aumentou MDA, MPO pancreática, MPO pulmonar e reduziu GSH em comparação com o grupo veículo (p ˂ 0,05). O 1,8-cineol 100, 200 e 400 mg/kg reduziu o edema pancreático (6; 27; 17 %), MDA (34; 29; 46 %), MPO pancreática (40; 55 e 78 %), MPO pulmonar (42; 45 e 22 %) e preservou GSH (62; 63 e 65 %). Estes achados sugerem que o 1,8-cineol pode prevenir a severidade da pancreatite aguda induzida por ceruleína em camundongos por meio de um mecanismo anti-inflamatório e antioxidantePancreatiteCeruletídeoEstresse OxidativoEfeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongosProtective effect of 1.8 cineol in acute pancreatitis induced in mice ceruleininfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisporreponame:Repositório Institucional da Universidade Federal do Ceará (UFC)instname:Universidade Federal do Ceará (UFC)instacron:UFCinfo:eu-repo/semantics/openAccessORIGINAL2013_dis_prlima.pdf2013_dis_prlima.pdfapplication/pdf1212941http://repositorio.ufc.br/bitstream/riufc/11957/1/2013_dis_prlima.pdfcfc24139d72f5da03ecbed2b1aee1d00MD51LICENSElicense.txtlicense.txttext/plain; charset=utf-81786http://repositorio.ufc.br/bitstream/riufc/11957/2/license.txt8c4401d3d14722a7ca2d07c782a1aab3MD52riufc/119572022-05-31 10:42:01.275oai:repositorio.ufc.br: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Repositório InstitucionalPUBhttp://www.repositorio.ufc.br/ri-oai/requestbu@ufc.br || repositorio@ufc.bropendoar:2022-05-31T13:42:01Repositório Institucional da Universidade Federal do Ceará (UFC) - Universidade Federal do Ceará (UFC)false
dc.title.pt_BR.fl_str_mv Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos
dc.title.en.pt_BR.fl_str_mv Protective effect of 1.8 cineol in acute pancreatitis induced in mice cerulein
title Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos
spellingShingle Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos
Lima, Patricia Rodrigues
Pancreatite
Ceruletídeo
Estresse Oxidativo
title_short Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos
title_full Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos
title_fullStr Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos
title_full_unstemmed Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos
title_sort Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos
author Lima, Patricia Rodrigues
author_facet Lima, Patricia Rodrigues
author_role author
dc.contributor.co-advisor.none.fl_str_mv Rao, Vietla Satyanarayana
dc.contributor.author.fl_str_mv Lima, Patricia Rodrigues
dc.contributor.advisor1.fl_str_mv Santos, Flávia Almeida
contributor_str_mv Santos, Flávia Almeida
dc.subject.por.fl_str_mv Pancreatite
Ceruletídeo
Estresse Oxidativo
topic Pancreatite
Ceruletídeo
Estresse Oxidativo
description Acute pancreatitis (AP) is an inflammatory condition in which pro-inflammatory mediators, oxidative stress and NF-kB signaling have a fundamental role. The 1,8-cineole, a monoterpene present in several plants species, is known for its antioxidant and anti-inflammatory potential. In order to verify its efficacy preventing AP, this study evaluated 1,8-cineole (100, 200 and 400 mg/kg, oral) on AP induced by cerulein (50 µg / kg / h × 5, i.p.) in Swiss mice. The 1,8-cineole was administrated one hour before the first injection of cerulein. Groups treated with vehicle or thalidomide were included as controls. Six hours later, blood samples were collected to determine blood levels of amylase, lipase and cytokines. The pancreas was removed for morphological examination, myeloperoxidase (MPO) and malondialdehyde (MDA) trials, changes in reduced glutathione (GSH) and for immunostaining of nuclear factor NF-κB. The right lung was removed for MPO trial. The 1,8-cineole reduced the histological damage and the expression of NF-κB induced by cerulein. Cerulein increased significantly amylase, lipase, TNF- α, IL1- β and IL-6, reducing IL-10. The 1,8-cineole 100, 200 and 400 mg/kg reversed significantly the damages caused by cerulein by reducing amylase (14; 16; 21 %), lipase (49; 48; 42 %), TNF-α (46; 66; 44 %), IL1-β (53; 45 e 67 %) e IL-6 (49; 40; 41 %) and enhanced IL-10 (34; 29 e 46 %), respectively. Cerulein produced pancreatic edema, increased MDA, pancreatic MPO, pulmonary MPO and decreased GSH comparing to the vehicle group (p < 0,05). The 1,8 cineole 100, 200 and 400 mg/kg reduced pancreatic edema (6; 27; 17%), MDA (34; 29; 46%), pancreatic MPO (40; 55 and 78 %), pulmonary MPO (42; 45 and 22 %) and preserved GSH (62; 63 and 65 %). These findings suggest that 1,8-cineol can prevent the severity of cerulein-induced acute pancreatitis in mice through an anti-inflammatory and antioxidant mechanisms.
publishDate 2013
dc.date.issued.fl_str_mv 2013
dc.date.accessioned.fl_str_mv 2015-05-11T13:14:13Z
dc.date.available.fl_str_mv 2015-05-11T13:14:13Z
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dc.identifier.citation.fl_str_mv LIMA, Patricia Rodrigues. Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos. Dissertação (Mestrado em Ciências Médicas) - Faculdade de Medicina, Universidade Federal do Ceará, Fortaleza, 2013.
dc.identifier.uri.fl_str_mv http://www.repositorio.ufc.br/handle/riufc/11957
identifier_str_mv LIMA, Patricia Rodrigues. Efeito protetor do 1,8 cineol na pancreatite aguda induzida por ceruleína em camundongos. Dissertação (Mestrado em Ciências Médicas) - Faculdade de Medicina, Universidade Federal do Ceará, Fortaleza, 2013.
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