Mecanismo de transporte iÃnico em Ãleo de coelho, induzido por microcistina LR de Microcystis aeruginos: ParticipaÃÃo de macrÃfagos,Il-1beta, TNFalpha e mediadores prÃ-inflamatÃrios

Detalhes bibliográficos
Autor(a) principal: George Chaves Jimenez
Data de Publicação: 2003
Tipo de documento: Tese
Idioma: por
Título da fonte: Biblioteca Digital de Teses e Dissertações da UFC
Texto Completo: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=29
Resumo: This work as main objective to evaluate the eletrogenic effect in preparations of Ãleum of rabbit fixes in chambers of Ãssing, in presence of supernatant of macrophages (S.MfS), stimulated with microcistin-LR (MCLR), of Microcystis aeruginosa. S.MfS estimulated with MCLR (3,2.10-7M; 9,6.10-7M e 3,2.10-6M), produces effect secretion, of the form dose-dependent; being that short circuit current (Isc), the secular chain variation (t) can be described for an equation of the type Isc = a . ekt for a correlation coefficient r = 0,9988 and Iscmaximo = 128,16 Â 14,54 ÂA . cm-2. Later, was observed that the metabolic processes associatesâ geneses of the FSI, from stimulated macrophages, require the participation of a protein G, sensible pertussis active toxin. It was also verified that inhibing of protÃic synthesis, proteases, phosfolipase A2, ciclooxigenases, lipoxigenases, synthesis TNF-a, and antagonists of the PAF, they had reduced the FSI synthesis. With the application of monoclonal antibodies, it was verified that interleukin-b (IL-1b), was the main FSI; as also, that macrophages stimulated with MCLR, in the concentrations above, produced IL-1b and TNF-a, of form dose-dependent. The pay-treatment of the ileum mucosal with bumetanide, indomethacin, tetrodotoxin and HOE, disclosed that the secretory effect, by means of stimulated action of the S.MfS with MCLR is dependent of the secretion of ions chloride, with the participation of PAF, prostaglandins and mediators of the enteric nervous system. With this effect, it associates reduction of the transepitelial resistance (Rte), also mediated for prostaglandins, TNF-a, and indirectly IL-1b. The analysis of the coefficient of Hurst, disclosed that these effect had not occurred of random form, but had involved significant alterations in the kinetic parameters of the eletrogÃnic effect, to the level of the ileum mucosal. Macrophages stimulated for MCLR, produces and liberate more TNF-a of that IL-1b, to the Constant taxes, being this a linked characteristic to the type of employed stimulation. It is concluded, therefore, that MCLR stimulates macrophages to produce substances that can act as intestinal secretion factor, to the level of the ileum mucosal, involving chloride canals, reduction of the Rte, requesting for this, the participation of pro-inflammatory mediators and the enteric nervous system.
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spelling info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/doctoralThesisMecanismo de transporte iÃnico em Ãleo de coelho, induzido por microcistina LR de Microcystis aeruginos: ParticipaÃÃo de macrÃfagos,Il-1beta, TNFalpha e mediadores prÃ-inflamatÃriosMechanism of ionic transport in ileum rabbit induced by microcystin-LR of Microcystis aeruginosa: Role of macrophages, IL-1b, TNF-a and pro-inflammatory mediators2003-05-09Aldo Ãngelo Moreira Lima09055339334http://lattes.cnpq.br/2153321168945169Marcos Hikari Toyama12069390870http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4763204P3Marcos FÃbio Gadelha Rocha44833504391http://lattes.cnpq.br/7504120886811849Helena Serra Azul Monteiro03277470300http://lattes.cnpq.br/3830155707659519Vietla Satyanarayana Rao21058550315http://lattes.cnpq.br/704654619105618788543951887http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4792668Z7George Chaves JimenezUniversidade Federal do CearÃPrograma de PÃs-GraduaÃÃo em FarmacologiaUFCBRMicrocystis Aeruginosa Microcistina-LR MacrÃfagos SecreÃÃo Intestinal Mediadores InflamatÃrios Interleucina-1b Coeficiente de Hurst e FractalMicrocystis Aeruginosa Microcystin-LR Macrophage Intestinal Secretion Pro-inflammatory Mediators Interleukin-1b Coefficient of Hurst and FractalFARMACOLOGIA CLINICAThis work as main objective to evaluate the eletrogenic effect in preparations of Ãleum of rabbit fixes in chambers of Ãssing, in presence of supernatant of macrophages (S.MfS), stimulated with microcistin-LR (MCLR), of Microcystis aeruginosa. S.MfS estimulated with MCLR (3,2.10-7M; 9,6.10-7M e 3,2.10-6M), produces effect secretion, of the form dose-dependent; being that short circuit current (Isc), the secular chain variation (t) can be described for an equation of the type Isc = a . ekt for a correlation coefficient r = 0,9988 and Iscmaximo = 128,16  14,54 ÂA . cm-2. Later, was observed that the metabolic processes associatesâ geneses of the FSI, from stimulated macrophages, require the participation of a protein G, sensible pertussis active toxin. It was also verified that inhibing of protÃic synthesis, proteases, phosfolipase A2, ciclooxigenases, lipoxigenases, synthesis TNF-a, and antagonists of the PAF, they had reduced the FSI synthesis. With the application of monoclonal antibodies, it was verified that interleukin-b (IL-1b), was the main FSI; as also, that macrophages stimulated with MCLR, in the concentrations above, produced IL-1b and TNF-a, of form dose-dependent. The pay-treatment of the ileum mucosal with bumetanide, indomethacin, tetrodotoxin and HOE, disclosed that the secretory effect, by means of stimulated action of the S.MfS with MCLR is dependent of the secretion of ions chloride, with the participation of PAF, prostaglandins and mediators of the enteric nervous system. With this effect, it associates reduction of the transepitelial resistance (Rte), also mediated for prostaglandins, TNF-a, and indirectly IL-1b. The analysis of the coefficient of Hurst, disclosed that these effect had not occurred of random form, but had involved significant alterations in the kinetic parameters of the eletrogÃnic effect, to the level of the ileum mucosal. Macrophages stimulated for MCLR, produces and liberate more TNF-a of that IL-1b, to the Constant taxes, being this a linked characteristic to the type of employed stimulation. It is concluded, therefore, that MCLR stimulates macrophages to produce substances that can act as intestinal secretion factor, to the level of the ileum mucosal, involving chloride canals, reduction of the Rte, requesting for this, the participation of pro-inflammatory mediators and the enteric nervous system.Este trabalho teve-se como principal objetivo, avaliar os efeitos eletrogÃnicos em preparaÃÃes de Ãleo de coelho fixadas em cÃmaras de Ãssing, em presenÃa de sobrenadante de macrÃfagos (S.MfS) estimulados com microcistina-LR MCLR de Microcystis aeruginosa. S.MfS estimulados com MCLR (3,2.10-7M; 9,6.10-7M e 3,2.10-6M), produz, de forma dose-dependente; sendo que a variaÃÃo temporal (t) da corrente de curto-circuito (Isc), pode ser descrita por uma equaÃÃo do tipo Isc = a . ekt; para um coeficiente de correlaÃÃo r = 0,9988 e Iscmaximo = 128,16  14,54 ÂÂcm-2. Posteriormente, observou-se que os processos metabÃlicos associados à gÃnese do fator deâ secreÃÃo intestinalâ (FSI), a partir de macrÃfagos estimulados, requer a participaÃÃo de uma proteÃna G sensÃvel à toxina pertusis ativa. Verificou-se tambÃm que inibidores de sÃntese protÃica, proteases, fosfolipase A2, cicloxigenases, lipoxigenases,; sÃntese de TNF-a e antagonista do PAF, reduziram a sÃntese de FSI. Com o emprego de anticorpos monoclonais, verificou-se que IL-1b era o principal FSI; como tambÃm, que macrÃfagos estimulados com MCLR, nas concentraÃÃes acima, reduziu IL-1b e TNF-a, de forma dose-dependente. O prÃ-tratamento da mucosa ileal com bumetanida, indometacina, tetrodotoxina e HOE, revelou que o efeito secretÃrio mediante aÃÃo do S.MfS estimulados com MCLR, à dependente da secreÃÃo de Ãons cloreto, com a participaÃÃo de PAF, prostaglandinas e mediadores do sistema nervoso entÃrico. A este efeito associa-se a diminuiÃÃo da resistÃncia transepitelial (Rte), tambÃm mediada por, prostaglandinas, PAF, TNF-a e, indiretamente, IL-1b. A anÃlise do coeficiente de Hurst (H), revelou que estes efeitos nÃo ocorreram ao acaso, mas envolveram alteraÃÃes significativas nos parÃmetros cinÃticos dos efeitos eletrogÃnicos, ao nÃvel da mucosa ileal. MacrÃfagos estimulados com MCLR produz e libera mais TNFa do que IL-1b, à taxas constantes ; sendo esta uma caracterÃstica atrelada ao tipo de estÃmulo empregado. Conclui-se, portanto, que MCLR estimula macrÃfagos a produzir substÃncias que podem atuar como fator de âsecreÃÃo intestinalâ ao nÃvel da mucosa ileal, envolvendo canais de cloreto, diminuiÃÃo de Rte; requisitando para isto, a participaÃÃo de mediadores prÃ-inflamatÃrios e do sistema nervoso entÃrico.CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superiorhttp://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=29application/pdfinfo:eu-repo/semantics/openAccessporreponame:Biblioteca Digital de Teses e Dissertações da UFCinstname:Universidade Federal do Cearáinstacron:UFC2019-01-21T11:13:06Zmail@mail.com -
dc.title.pt.fl_str_mv Mecanismo de transporte iÃnico em Ãleo de coelho, induzido por microcistina LR de Microcystis aeruginos: ParticipaÃÃo de macrÃfagos,Il-1beta, TNFalpha e mediadores prÃ-inflamatÃrios
dc.title.alternative.en.fl_str_mv Mechanism of ionic transport in ileum rabbit induced by microcystin-LR of Microcystis aeruginosa: Role of macrophages, IL-1b, TNF-a and pro-inflammatory mediators
title Mecanismo de transporte iÃnico em Ãleo de coelho, induzido por microcistina LR de Microcystis aeruginos: ParticipaÃÃo de macrÃfagos,Il-1beta, TNFalpha e mediadores prÃ-inflamatÃrios
spellingShingle Mecanismo de transporte iÃnico em Ãleo de coelho, induzido por microcistina LR de Microcystis aeruginos: ParticipaÃÃo de macrÃfagos,Il-1beta, TNFalpha e mediadores prÃ-inflamatÃrios
George Chaves Jimenez
Microcystis Aeruginosa
Microcistina-LR
MacrÃfagos
SecreÃÃo Intestinal
Mediadores InflamatÃrios
Interleucina-1b
Coeficiente de Hurst e Fractal
Microcystis Aeruginosa
Microcystin-LR Macrophage
Intestinal Secretion
Pro-inflammatory Mediators
Interleukin-1b
Coefficient of Hurst and Fractal
FARMACOLOGIA CLINICA
title_short Mecanismo de transporte iÃnico em Ãleo de coelho, induzido por microcistina LR de Microcystis aeruginos: ParticipaÃÃo de macrÃfagos,Il-1beta, TNFalpha e mediadores prÃ-inflamatÃrios
title_full Mecanismo de transporte iÃnico em Ãleo de coelho, induzido por microcistina LR de Microcystis aeruginos: ParticipaÃÃo de macrÃfagos,Il-1beta, TNFalpha e mediadores prÃ-inflamatÃrios
title_fullStr Mecanismo de transporte iÃnico em Ãleo de coelho, induzido por microcistina LR de Microcystis aeruginos: ParticipaÃÃo de macrÃfagos,Il-1beta, TNFalpha e mediadores prÃ-inflamatÃrios
title_full_unstemmed Mecanismo de transporte iÃnico em Ãleo de coelho, induzido por microcistina LR de Microcystis aeruginos: ParticipaÃÃo de macrÃfagos,Il-1beta, TNFalpha e mediadores prÃ-inflamatÃrios
title_sort Mecanismo de transporte iÃnico em Ãleo de coelho, induzido por microcistina LR de Microcystis aeruginos: ParticipaÃÃo de macrÃfagos,Il-1beta, TNFalpha e mediadores prÃ-inflamatÃrios
author George Chaves Jimenez
author_facet George Chaves Jimenez
author_role author
dc.contributor.advisor1.fl_str_mv Aldo Ãngelo Moreira Lima
dc.contributor.advisor1ID.fl_str_mv 09055339334
dc.contributor.advisor1Lattes.fl_str_mv http://lattes.cnpq.br/2153321168945169
dc.contributor.referee1.fl_str_mv Marcos Hikari Toyama
dc.contributor.referee1ID.fl_str_mv 12069390870
dc.contributor.referee1Lattes.fl_str_mv http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4763204P3
dc.contributor.referee2.fl_str_mv Marcos FÃbio Gadelha Rocha
dc.contributor.referee2ID.fl_str_mv 44833504391
dc.contributor.referee2Lattes.fl_str_mv http://lattes.cnpq.br/7504120886811849
dc.contributor.referee3.fl_str_mv Helena Serra Azul Monteiro
dc.contributor.referee3ID.fl_str_mv 03277470300
dc.contributor.referee3Lattes.fl_str_mv http://lattes.cnpq.br/3830155707659519
dc.contributor.referee4.fl_str_mv Vietla Satyanarayana Rao
dc.contributor.referee4ID.fl_str_mv 21058550315
dc.contributor.referee4Lattes.fl_str_mv http://lattes.cnpq.br/7046546191056187
dc.contributor.authorID.fl_str_mv 88543951887
dc.contributor.authorLattes.fl_str_mv http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4792668Z7
dc.contributor.author.fl_str_mv George Chaves Jimenez
contributor_str_mv Aldo Ãngelo Moreira Lima
Marcos Hikari Toyama
Marcos FÃbio Gadelha Rocha
Helena Serra Azul Monteiro
Vietla Satyanarayana Rao
dc.subject.por.fl_str_mv Microcystis Aeruginosa
Microcistina-LR
MacrÃfagos
SecreÃÃo Intestinal
Mediadores InflamatÃrios
Interleucina-1b
Coeficiente de Hurst e Fractal
topic Microcystis Aeruginosa
Microcistina-LR
MacrÃfagos
SecreÃÃo Intestinal
Mediadores InflamatÃrios
Interleucina-1b
Coeficiente de Hurst e Fractal
Microcystis Aeruginosa
Microcystin-LR Macrophage
Intestinal Secretion
Pro-inflammatory Mediators
Interleukin-1b
Coefficient of Hurst and Fractal
FARMACOLOGIA CLINICA
dc.subject.eng.fl_str_mv Microcystis Aeruginosa
Microcystin-LR Macrophage
Intestinal Secretion
Pro-inflammatory Mediators
Interleukin-1b
Coefficient of Hurst and Fractal
dc.subject.cnpq.fl_str_mv FARMACOLOGIA CLINICA
dc.description.sponsorship.fl_txt_mv CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
dc.description.abstract.por.fl_txt_mv This work as main objective to evaluate the eletrogenic effect in preparations of Ãleum of rabbit fixes in chambers of Ãssing, in presence of supernatant of macrophages (S.MfS), stimulated with microcistin-LR (MCLR), of Microcystis aeruginosa. S.MfS estimulated with MCLR (3,2.10-7M; 9,6.10-7M e 3,2.10-6M), produces effect secretion, of the form dose-dependent; being that short circuit current (Isc), the secular chain variation (t) can be described for an equation of the type Isc = a . ekt for a correlation coefficient r = 0,9988 and Iscmaximo = 128,16 Â 14,54 ÂA . cm-2. Later, was observed that the metabolic processes associatesâ geneses of the FSI, from stimulated macrophages, require the participation of a protein G, sensible pertussis active toxin. It was also verified that inhibing of protÃic synthesis, proteases, phosfolipase A2, ciclooxigenases, lipoxigenases, synthesis TNF-a, and antagonists of the PAF, they had reduced the FSI synthesis. With the application of monoclonal antibodies, it was verified that interleukin-b (IL-1b), was the main FSI; as also, that macrophages stimulated with MCLR, in the concentrations above, produced IL-1b and TNF-a, of form dose-dependent. The pay-treatment of the ileum mucosal with bumetanide, indomethacin, tetrodotoxin and HOE, disclosed that the secretory effect, by means of stimulated action of the S.MfS with MCLR is dependent of the secretion of ions chloride, with the participation of PAF, prostaglandins and mediators of the enteric nervous system. With this effect, it associates reduction of the transepitelial resistance (Rte), also mediated for prostaglandins, TNF-a, and indirectly IL-1b. The analysis of the coefficient of Hurst, disclosed that these effect had not occurred of random form, but had involved significant alterations in the kinetic parameters of the eletrogÃnic effect, to the level of the ileum mucosal. Macrophages stimulated for MCLR, produces and liberate more TNF-a of that IL-1b, to the Constant taxes, being this a linked characteristic to the type of employed stimulation. It is concluded, therefore, that MCLR stimulates macrophages to produce substances that can act as intestinal secretion factor, to the level of the ileum mucosal, involving chloride canals, reduction of the Rte, requesting for this, the participation of pro-inflammatory mediators and the enteric nervous system.
Este trabalho teve-se como principal objetivo, avaliar os efeitos eletrogÃnicos em preparaÃÃes de Ãleo de coelho fixadas em cÃmaras de Ãssing, em presenÃa de sobrenadante de macrÃfagos (S.MfS) estimulados com microcistina-LR MCLR de Microcystis aeruginosa. S.MfS estimulados com MCLR (3,2.10-7M; 9,6.10-7M e 3,2.10-6M), produz, de forma dose-dependente; sendo que a variaÃÃo temporal (t) da corrente de curto-circuito (Isc), pode ser descrita por uma equaÃÃo do tipo Isc = a . ekt; para um coeficiente de correlaÃÃo r = 0,9988 e Iscmaximo = 128,16  14,54 ÂÂcm-2. Posteriormente, observou-se que os processos metabÃlicos associados à gÃnese do fator deâ secreÃÃo intestinalâ (FSI), a partir de macrÃfagos estimulados, requer a participaÃÃo de uma proteÃna G sensÃvel à toxina pertusis ativa. Verificou-se tambÃm que inibidores de sÃntese protÃica, proteases, fosfolipase A2, cicloxigenases, lipoxigenases,; sÃntese de TNF-a e antagonista do PAF, reduziram a sÃntese de FSI. Com o emprego de anticorpos monoclonais, verificou-se que IL-1b era o principal FSI; como tambÃm, que macrÃfagos estimulados com MCLR, nas concentraÃÃes acima, reduziu IL-1b e TNF-a, de forma dose-dependente. O prÃ-tratamento da mucosa ileal com bumetanida, indometacina, tetrodotoxina e HOE, revelou que o efeito secretÃrio mediante aÃÃo do S.MfS estimulados com MCLR, à dependente da secreÃÃo de Ãons cloreto, com a participaÃÃo de PAF, prostaglandinas e mediadores do sistema nervoso entÃrico. A este efeito associa-se a diminuiÃÃo da resistÃncia transepitelial (Rte), tambÃm mediada por, prostaglandinas, PAF, TNF-a e, indiretamente, IL-1b. A anÃlise do coeficiente de Hurst (H), revelou que estes efeitos nÃo ocorreram ao acaso, mas envolveram alteraÃÃes significativas nos parÃmetros cinÃticos dos efeitos eletrogÃnicos, ao nÃvel da mucosa ileal. MacrÃfagos estimulados com MCLR produz e libera mais TNFa do que IL-1b, à taxas constantes ; sendo esta uma caracterÃstica atrelada ao tipo de estÃmulo empregado. Conclui-se, portanto, que MCLR estimula macrÃfagos a produzir substÃncias que podem atuar como fator de âsecreÃÃo intestinalâ ao nÃvel da mucosa ileal, envolvendo canais de cloreto, diminuiÃÃo de Rte; requisitando para isto, a participaÃÃo de mediadores prÃ-inflamatÃrios e do sistema nervoso entÃrico.
description This work as main objective to evaluate the eletrogenic effect in preparations of Ãleum of rabbit fixes in chambers of Ãssing, in presence of supernatant of macrophages (S.MfS), stimulated with microcistin-LR (MCLR), of Microcystis aeruginosa. S.MfS estimulated with MCLR (3,2.10-7M; 9,6.10-7M e 3,2.10-6M), produces effect secretion, of the form dose-dependent; being that short circuit current (Isc), the secular chain variation (t) can be described for an equation of the type Isc = a . ekt for a correlation coefficient r = 0,9988 and Iscmaximo = 128,16 Â 14,54 ÂA . cm-2. Later, was observed that the metabolic processes associatesâ geneses of the FSI, from stimulated macrophages, require the participation of a protein G, sensible pertussis active toxin. It was also verified that inhibing of protÃic synthesis, proteases, phosfolipase A2, ciclooxigenases, lipoxigenases, synthesis TNF-a, and antagonists of the PAF, they had reduced the FSI synthesis. With the application of monoclonal antibodies, it was verified that interleukin-b (IL-1b), was the main FSI; as also, that macrophages stimulated with MCLR, in the concentrations above, produced IL-1b and TNF-a, of form dose-dependent. The pay-treatment of the ileum mucosal with bumetanide, indomethacin, tetrodotoxin and HOE, disclosed that the secretory effect, by means of stimulated action of the S.MfS with MCLR is dependent of the secretion of ions chloride, with the participation of PAF, prostaglandins and mediators of the enteric nervous system. With this effect, it associates reduction of the transepitelial resistance (Rte), also mediated for prostaglandins, TNF-a, and indirectly IL-1b. The analysis of the coefficient of Hurst, disclosed that these effect had not occurred of random form, but had involved significant alterations in the kinetic parameters of the eletrogÃnic effect, to the level of the ileum mucosal. Macrophages stimulated for MCLR, produces and liberate more TNF-a of that IL-1b, to the Constant taxes, being this a linked characteristic to the type of employed stimulation. It is concluded, therefore, that MCLR stimulates macrophages to produce substances that can act as intestinal secretion factor, to the level of the ileum mucosal, involving chloride canals, reduction of the Rte, requesting for this, the participation of pro-inflammatory mediators and the enteric nervous system.
publishDate 2003
dc.date.issued.fl_str_mv 2003-05-09
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/doctoralThesis
status_str publishedVersion
format doctoralThesis
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url http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=29
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language por
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
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dc.publisher.none.fl_str_mv Universidade Federal do CearÃ
dc.publisher.program.fl_str_mv Programa de PÃs-GraduaÃÃo em Farmacologia
dc.publisher.initials.fl_str_mv UFC
dc.publisher.country.fl_str_mv BR
publisher.none.fl_str_mv Universidade Federal do CearÃ
dc.source.none.fl_str_mv reponame:Biblioteca Digital de Teses e Dissertações da UFC
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instname_str Universidade Federal do Ceará
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