Effect anti-necrotic of ConA and ConBr lectins in pancreatic acinar cell injury induced by bile salt, alcohol, and palmitoleic acid: involvement of the lectin domain
Autor(a) principal: | |
---|---|
Data de Publicação: | 2015 |
Tipo de documento: | Dissertação |
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=13880 |
Resumo: | Acute pancreatitis is an inflammatory disease of the pancreas which involves a complex sequence of pathophysiological events, many of which are still unknown. Recent data give more importance to the events that happen within the pancreatic cell. The severity and duration of the stimulus applied to pancreatic acinar cells may lead to apoptosis or necrosis. A large number of studies have demonstrated that the lectin of Canavalia ensiformis (ConA) and Canavalia brasiliensis (ConBr) induce cell death by apoptosis in various cell types. However there are no studies on its anti-necrotic effects. Thus, we investigated the effects of ConA and ConBr concerning the death of pancreatic acinar cells, induced by the main triggers of acute pancreatitis. The acinar cells were isolated from the pancreas of male Swiss mice. The cells were pre-incubated with ConA and ConBr for 1h followed by the induction of cell damage by SATC, ethanol or APO administration for 30 min (room temperature, RT). To evaluate the role of the lectin domain of ConBr and ConA, the lectins were preincubated for 1h at 37ÂC with its alpha-methyl-mannoside (α-MM) ligand sugar, or with a nonbinding sugar, D-galactose, both at a concentration of 0.2M, prior to experimental protocols. All groups were incubated for 5 minutes with the nuclear marker Hoechst 33342 (50 Âg/ml) and with the necrosis marker, propidium iodide (PI; 10 Âg/ml). In another analysis, ConA and ConBr conjugated to fluorescein isothiocyanate (FITC) were incubated for 1h (RT) with the acinar cells. To evaluate the effect of ConA and ConBr effect on mitochondrial membrane potential (ΔѰm) of pancreatic acinar cells under administration of SATC, ethanol or APO, the cells were stained with Hoechst 33342, and tetramethylrhodamine methyl ester (TMRM, fluorescent dye that is readily sequestered by active mitochondria). All analyzes were performed using confocal microscope FluoViewTM 1000 - Olympus. The results showed that the SATC, ethanol and APO groups caused significant necrosis on cells compared to control groups, and pretreatment ConBr and ConA caused a significant protection against harmful necrosis caused by all three agents. When lectins were complexed to their α-MM ligand sugar, this protective effect was significantly reversed; not being changed, however, by no specific sugar D-galactose, suggesting a participation of the lectin domain in protective effect. Lectins conjugated with FITC showed a marking on acinar cells at the level of membrane, confirming its interaction with carbohydrates present on the surface of these cells. In the analysis of mitochondrial potential, SATC, ethanol and mainly APO triggered intense depolarization of ΔѰm of pancreatic acinar cells. Pretreatment with ConA prevented mitochondrial dysfunction in all injury models, however ConBr prevented this injury caused by a dysfunction in SATC and ethanol, without changing the dysfunction caused by APO. Given the above, Con A and Con Br protect pancreatic acinar cells against necrosis induced by sulfated taurolithocholic acid, ethanol and APO with its effects mediated by lectin domain, beyond of the maintenance the integrity of the mitochondrial membrane of pancreatic cell, determinant factor to prevent the course of necrosis in acute pancreatitis. |
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info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisEffect anti-necrotic of ConA and ConBr lectins in pancreatic acinar cell injury induced by bile salt, alcohol, and palmitoleic acid: involvement of the lectin domainEfeito antinecrÃtico das lectinas ConA e ConBr na lesÃo de cÃlulas acinares pancreÃticas induzida por sais biliares, Ãlcool e Ãcido palmitoleico: envolvimento do domÃnio lectÃnico2015-01-19Pedro Marcos Gomes Soares74208497300http://lattes.cnpq.br/6897520172728361Reinaldo Barreto OriÃ42657946372http://lattes.cnpq.br/3091742095568302Alana de Freitas Pires92567533320http://lattes.cnpq.br/097964763963233503731536358http://lattes.cnpq.br/8755037347949197Samara Rodrigues Bonfim DamascenoUniversidade Federal do CearÃPrograma de PÃs-GraduaÃÃo em FarmacologiaUFCBRFARMACOLOGIAAcute pancreatitis is an inflammatory disease of the pancreas which involves a complex sequence of pathophysiological events, many of which are still unknown. Recent data give more importance to the events that happen within the pancreatic cell. The severity and duration of the stimulus applied to pancreatic acinar cells may lead to apoptosis or necrosis. A large number of studies have demonstrated that the lectin of Canavalia ensiformis (ConA) and Canavalia brasiliensis (ConBr) induce cell death by apoptosis in various cell types. However there are no studies on its anti-necrotic effects. Thus, we investigated the effects of ConA and ConBr concerning the death of pancreatic acinar cells, induced by the main triggers of acute pancreatitis. The acinar cells were isolated from the pancreas of male Swiss mice. The cells were pre-incubated with ConA and ConBr for 1h followed by the induction of cell damage by SATC, ethanol or APO administration for 30 min (room temperature, RT). To evaluate the role of the lectin domain of ConBr and ConA, the lectins were preincubated for 1h at 37ÂC with its alpha-methyl-mannoside (α-MM) ligand sugar, or with a nonbinding sugar, D-galactose, both at a concentration of 0.2M, prior to experimental protocols. All groups were incubated for 5 minutes with the nuclear marker Hoechst 33342 (50 Âg/ml) and with the necrosis marker, propidium iodide (PI; 10 Âg/ml). In another analysis, ConA and ConBr conjugated to fluorescein isothiocyanate (FITC) were incubated for 1h (RT) with the acinar cells. To evaluate the effect of ConA and ConBr effect on mitochondrial membrane potential (ΔѰm) of pancreatic acinar cells under administration of SATC, ethanol or APO, the cells were stained with Hoechst 33342, and tetramethylrhodamine methyl ester (TMRM, fluorescent dye that is readily sequestered by active mitochondria). All analyzes were performed using confocal microscope FluoViewTM 1000 - Olympus. The results showed that the SATC, ethanol and APO groups caused significant necrosis on cells compared to control groups, and pretreatment ConBr and ConA caused a significant protection against harmful necrosis caused by all three agents. When lectins were complexed to their α-MM ligand sugar, this protective effect was significantly reversed; not being changed, however, by no specific sugar D-galactose, suggesting a participation of the lectin domain in protective effect. Lectins conjugated with FITC showed a marking on acinar cells at the level of membrane, confirming its interaction with carbohydrates present on the surface of these cells. In the analysis of mitochondrial potential, SATC, ethanol and mainly APO triggered intense depolarization of ΔѰm of pancreatic acinar cells. Pretreatment with ConA prevented mitochondrial dysfunction in all injury models, however ConBr prevented this injury caused by a dysfunction in SATC and ethanol, without changing the dysfunction caused by APO. Given the above, Con A and Con Br protect pancreatic acinar cells against necrosis induced by sulfated taurolithocholic acid, ethanol and APO with its effects mediated by lectin domain, beyond of the maintenance the integrity of the mitochondrial membrane of pancreatic cell, determinant factor to prevent the course of necrosis in acute pancreatitis.A pancreatite aguda à uma doenÃa inflamatÃria do pÃncreas que envolve uma sequÃncia complexa de eventos fisiopatolÃgicos, muitos dos quais ainda desconhecidos. Dados recentes atribuem maior importÃncia aos eventos que aconteceriam no interior da cÃlula pancreÃtica. A gravidade e a duraÃÃo do estÃmulo aplicado Ãs cÃlulas acinares pancreÃticas podem levar à apoptose ou à necrose. Um grande nÃmero de estudos demonstraram que as lectinas de Canavalia ensiformis (ConA) e Canavalia brasiliensis (ConBr) induzem morte celular por apoptose em diversos tipos de cÃlulas. Contudo nÃo hà estudos sobre seus efeitos anti-necrÃticos. Dessa forma, investigamos os efeitos de ConA e ConBr frente à morte de cÃlulas acinares pancreÃticas, induzida pelos principais desencadeadores da pancreatite aguda. As cÃlulas acinares foram isoladas de pÃncreas de camundongos Swiss machos. As cÃlulas foram previamente incubadas durante 1h com ConA (200 Âg/ml) e ConBr (200 Âg/ml) seguido da induÃÃo das lesÃes celulares pela administraÃÃo de SATC (500ÂM), etanol (850mM) ou APO (100 ÂM) durante 30 min (T.A). Para avaliar a participaÃÃo do domÃnio lectÃnico de ConA e ConBr, as lectinas foram previamente incubadas, durante 1h a 37ÂC, com seu aÃÃcar ligante α-metil-manosÃdeo (α-MM), ou com um aÃÃcar nÃo ligante, D-galactose, ambos na concentraÃÃo de 0,2M, antes dos protocolos experimentais. Todos os grupos foram incubados por 5 minutos com o marcador nuclear Hoechst 33342 (50 Âg/ml) e com o marcador de necrose iodeto de propÃdeo (IP; 10 Âg/ml). Em outra anÃlise, ConA e ConBr conjugadas ao isotiocianato de fluoresceÃna (FITC) foram incubadas durante 1h (T.A), com as cÃlulas acinares. Para a avaliaÃÃo do efeito de ConA e ConBr no potencial de membrana mitocondrial (ΔѰm) de cÃlulas acinares pancreÃticas sob administraÃÃo de SATC, etanol ou APO, as cÃlulas foram marcadas com Hoechst 33342 e tetrametilrodamina-metilÃster (TMRM, corante fluorescente que à prontamente sequestrado pela mitocÃndria ativa). Todas as anÃlises foram realizadas no microscÃpio confocal FluoViewTM 1000 â Olympus. Os resultados mostraram que os grupos SATC, etanol e APO causaram necrose significativa Ãs cÃlulas, quando comparado com os grupos controles e que o prÃ-tratamento de ConA e ConBr promoveu proteÃÃo significativa (p < 0,05) contra a necrose causada pelos trÃs agentes lesivos. Quando as lectinas foram complexadas ao seu aÃÃcar ligante, α-MM, este efeito protetor foi significativamente revertido (p < 0,05); nÃo sendo alterado, porÃm, pelo aÃÃcar nÃo especÃfico D-galactose, evidenciando a participaÃÃo do domÃnio lectÃnico no seu efeito protetor. As lectinas conjugadas com FITC evidenciaram uma marcaÃÃo nas cÃlulas acinares a nÃvel de membrana, confirmando a sua interaÃÃo com carboidratos presentes na superfÃcie dessas cÃlulas. Na anÃlise do potencial mitocondrial, SATC, etanol e principalmente APO desencadearam intensa despolarizaÃÃo do ΔѰm das cÃlulas acinares pancreÃticas. O prÃ-tratamento com ConA preveniu (p < 0,05) a disfunÃÃo mitocondrial em todos os modelos de lesÃo, contudo ConBr preveniu essa disfunÃÃo na lesÃo causada por SATC e etanol (p < 0,05), sem alterar a disfunÃÃo causada por APO. Diante do exposto, ConA e ConBr protegem cÃlulas acinares pancreÃticas contra a necrose induzida por Ãcido taurolitocÃlico sulfatado, etanol e APO, tendo seus efeitos mediados pelo domÃnio lectÃnico, alÃm da manutenÃÃo da integridade da membrana mitocondrial da cÃlula pancreÃtica, fator determinante para evitar o curso da necrose na pancreatite aguda.Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgicohttp://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=13880application/pdfinfo:eu-repo/semantics/openAccessporreponame:Biblioteca Digital de Teses e Dissertações da UFCinstname:Universidade Federal do Cearáinstacron:UFC2019-01-21T11:27:05Zmail@mail.com - |
dc.title.en.fl_str_mv |
Effect anti-necrotic of ConA and ConBr lectins in pancreatic acinar cell injury induced by bile salt, alcohol, and palmitoleic acid: involvement of the lectin domain |
dc.title.alternative.pt.fl_str_mv |
Efeito antinecrÃtico das lectinas ConA e ConBr na lesÃo de cÃlulas acinares pancreÃticas induzida por sais biliares, Ãlcool e Ãcido palmitoleico: envolvimento do domÃnio lectÃnico |
title |
Effect anti-necrotic of ConA and ConBr lectins in pancreatic acinar cell injury induced by bile salt, alcohol, and palmitoleic acid: involvement of the lectin domain |
spellingShingle |
Effect anti-necrotic of ConA and ConBr lectins in pancreatic acinar cell injury induced by bile salt, alcohol, and palmitoleic acid: involvement of the lectin domain Samara Rodrigues Bonfim Damasceno FARMACOLOGIA |
title_short |
Effect anti-necrotic of ConA and ConBr lectins in pancreatic acinar cell injury induced by bile salt, alcohol, and palmitoleic acid: involvement of the lectin domain |
title_full |
Effect anti-necrotic of ConA and ConBr lectins in pancreatic acinar cell injury induced by bile salt, alcohol, and palmitoleic acid: involvement of the lectin domain |
title_fullStr |
Effect anti-necrotic of ConA and ConBr lectins in pancreatic acinar cell injury induced by bile salt, alcohol, and palmitoleic acid: involvement of the lectin domain |
title_full_unstemmed |
Effect anti-necrotic of ConA and ConBr lectins in pancreatic acinar cell injury induced by bile salt, alcohol, and palmitoleic acid: involvement of the lectin domain |
title_sort |
Effect anti-necrotic of ConA and ConBr lectins in pancreatic acinar cell injury induced by bile salt, alcohol, and palmitoleic acid: involvement of the lectin domain |
author |
Samara Rodrigues Bonfim Damasceno |
author_facet |
Samara Rodrigues Bonfim Damasceno |
author_role |
author |
dc.contributor.advisor1.fl_str_mv |
Pedro Marcos Gomes Soares |
dc.contributor.advisor1ID.fl_str_mv |
74208497300 |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/6897520172728361 |
dc.contributor.referee1.fl_str_mv |
Reinaldo Barreto Orià |
dc.contributor.referee1ID.fl_str_mv |
42657946372 |
dc.contributor.referee1Lattes.fl_str_mv |
http://lattes.cnpq.br/3091742095568302 |
dc.contributor.referee2.fl_str_mv |
Alana de Freitas Pires |
dc.contributor.referee2ID.fl_str_mv |
92567533320 |
dc.contributor.referee2Lattes.fl_str_mv |
http://lattes.cnpq.br/0979647639632335 |
dc.contributor.authorID.fl_str_mv |
03731536358 |
dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/8755037347949197 |
dc.contributor.author.fl_str_mv |
Samara Rodrigues Bonfim Damasceno |
contributor_str_mv |
Pedro Marcos Gomes Soares Reinaldo Barreto Orià Alana de Freitas Pires |
dc.subject.cnpq.fl_str_mv |
FARMACOLOGIA |
topic |
FARMACOLOGIA |
dc.description.sponsorship.fl_txt_mv |
Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico |
dc.description.abstract.por.fl_txt_mv |
Acute pancreatitis is an inflammatory disease of the pancreas which involves a complex sequence of pathophysiological events, many of which are still unknown. Recent data give more importance to the events that happen within the pancreatic cell. The severity and duration of the stimulus applied to pancreatic acinar cells may lead to apoptosis or necrosis. A large number of studies have demonstrated that the lectin of Canavalia ensiformis (ConA) and Canavalia brasiliensis (ConBr) induce cell death by apoptosis in various cell types. However there are no studies on its anti-necrotic effects. Thus, we investigated the effects of ConA and ConBr concerning the death of pancreatic acinar cells, induced by the main triggers of acute pancreatitis. The acinar cells were isolated from the pancreas of male Swiss mice. The cells were pre-incubated with ConA and ConBr for 1h followed by the induction of cell damage by SATC, ethanol or APO administration for 30 min (room temperature, RT). To evaluate the role of the lectin domain of ConBr and ConA, the lectins were preincubated for 1h at 37ÂC with its alpha-methyl-mannoside (α-MM) ligand sugar, or with a nonbinding sugar, D-galactose, both at a concentration of 0.2M, prior to experimental protocols. All groups were incubated for 5 minutes with the nuclear marker Hoechst 33342 (50 Âg/ml) and with the necrosis marker, propidium iodide (PI; 10 Âg/ml). In another analysis, ConA and ConBr conjugated to fluorescein isothiocyanate (FITC) were incubated for 1h (RT) with the acinar cells. To evaluate the effect of ConA and ConBr effect on mitochondrial membrane potential (ΔѰm) of pancreatic acinar cells under administration of SATC, ethanol or APO, the cells were stained with Hoechst 33342, and tetramethylrhodamine methyl ester (TMRM, fluorescent dye that is readily sequestered by active mitochondria). All analyzes were performed using confocal microscope FluoViewTM 1000 - Olympus. The results showed that the SATC, ethanol and APO groups caused significant necrosis on cells compared to control groups, and pretreatment ConBr and ConA caused a significant protection against harmful necrosis caused by all three agents. When lectins were complexed to their α-MM ligand sugar, this protective effect was significantly reversed; not being changed, however, by no specific sugar D-galactose, suggesting a participation of the lectin domain in protective effect. Lectins conjugated with FITC showed a marking on acinar cells at the level of membrane, confirming its interaction with carbohydrates present on the surface of these cells. In the analysis of mitochondrial potential, SATC, ethanol and mainly APO triggered intense depolarization of ΔѰm of pancreatic acinar cells. Pretreatment with ConA prevented mitochondrial dysfunction in all injury models, however ConBr prevented this injury caused by a dysfunction in SATC and ethanol, without changing the dysfunction caused by APO. Given the above, Con A and Con Br protect pancreatic acinar cells against necrosis induced by sulfated taurolithocholic acid, ethanol and APO with its effects mediated by lectin domain, beyond of the maintenance the integrity of the mitochondrial membrane of pancreatic cell, determinant factor to prevent the course of necrosis in acute pancreatitis. A pancreatite aguda à uma doenÃa inflamatÃria do pÃncreas que envolve uma sequÃncia complexa de eventos fisiopatolÃgicos, muitos dos quais ainda desconhecidos. Dados recentes atribuem maior importÃncia aos eventos que aconteceriam no interior da cÃlula pancreÃtica. A gravidade e a duraÃÃo do estÃmulo aplicado Ãs cÃlulas acinares pancreÃticas podem levar à apoptose ou à necrose. Um grande nÃmero de estudos demonstraram que as lectinas de Canavalia ensiformis (ConA) e Canavalia brasiliensis (ConBr) induzem morte celular por apoptose em diversos tipos de cÃlulas. Contudo nÃo hà estudos sobre seus efeitos anti-necrÃticos. Dessa forma, investigamos os efeitos de ConA e ConBr frente à morte de cÃlulas acinares pancreÃticas, induzida pelos principais desencadeadores da pancreatite aguda. As cÃlulas acinares foram isoladas de pÃncreas de camundongos Swiss machos. As cÃlulas foram previamente incubadas durante 1h com ConA (200 Âg/ml) e ConBr (200 Âg/ml) seguido da induÃÃo das lesÃes celulares pela administraÃÃo de SATC (500ÂM), etanol (850mM) ou APO (100 ÂM) durante 30 min (T.A). Para avaliar a participaÃÃo do domÃnio lectÃnico de ConA e ConBr, as lectinas foram previamente incubadas, durante 1h a 37ÂC, com seu aÃÃcar ligante α-metil-manosÃdeo (α-MM), ou com um aÃÃcar nÃo ligante, D-galactose, ambos na concentraÃÃo de 0,2M, antes dos protocolos experimentais. Todos os grupos foram incubados por 5 minutos com o marcador nuclear Hoechst 33342 (50 Âg/ml) e com o marcador de necrose iodeto de propÃdeo (IP; 10 Âg/ml). Em outra anÃlise, ConA e ConBr conjugadas ao isotiocianato de fluoresceÃna (FITC) foram incubadas durante 1h (T.A), com as cÃlulas acinares. Para a avaliaÃÃo do efeito de ConA e ConBr no potencial de membrana mitocondrial (ΔѰm) de cÃlulas acinares pancreÃticas sob administraÃÃo de SATC, etanol ou APO, as cÃlulas foram marcadas com Hoechst 33342 e tetrametilrodamina-metilÃster (TMRM, corante fluorescente que à prontamente sequestrado pela mitocÃndria ativa). Todas as anÃlises foram realizadas no microscÃpio confocal FluoViewTM 1000 â Olympus. Os resultados mostraram que os grupos SATC, etanol e APO causaram necrose significativa Ãs cÃlulas, quando comparado com os grupos controles e que o prÃ-tratamento de ConA e ConBr promoveu proteÃÃo significativa (p < 0,05) contra a necrose causada pelos trÃs agentes lesivos. Quando as lectinas foram complexadas ao seu aÃÃcar ligante, α-MM, este efeito protetor foi significativamente revertido (p < 0,05); nÃo sendo alterado, porÃm, pelo aÃÃcar nÃo especÃfico D-galactose, evidenciando a participaÃÃo do domÃnio lectÃnico no seu efeito protetor. As lectinas conjugadas com FITC evidenciaram uma marcaÃÃo nas cÃlulas acinares a nÃvel de membrana, confirmando a sua interaÃÃo com carboidratos presentes na superfÃcie dessas cÃlulas. Na anÃlise do potencial mitocondrial, SATC, etanol e principalmente APO desencadearam intensa despolarizaÃÃo do ΔѰm das cÃlulas acinares pancreÃticas. O prÃ-tratamento com ConA preveniu (p < 0,05) a disfunÃÃo mitocondrial em todos os modelos de lesÃo, contudo ConBr preveniu essa disfunÃÃo na lesÃo causada por SATC e etanol (p < 0,05), sem alterar a disfunÃÃo causada por APO. Diante do exposto, ConA e ConBr protegem cÃlulas acinares pancreÃticas contra a necrose induzida por Ãcido taurolitocÃlico sulfatado, etanol e APO, tendo seus efeitos mediados pelo domÃnio lectÃnico, alÃm da manutenÃÃo da integridade da membrana mitocondrial da cÃlula pancreÃtica, fator determinante para evitar o curso da necrose na pancreatite aguda. |
description |
Acute pancreatitis is an inflammatory disease of the pancreas which involves a complex sequence of pathophysiological events, many of which are still unknown. Recent data give more importance to the events that happen within the pancreatic cell. The severity and duration of the stimulus applied to pancreatic acinar cells may lead to apoptosis or necrosis. A large number of studies have demonstrated that the lectin of Canavalia ensiformis (ConA) and Canavalia brasiliensis (ConBr) induce cell death by apoptosis in various cell types. However there are no studies on its anti-necrotic effects. Thus, we investigated the effects of ConA and ConBr concerning the death of pancreatic acinar cells, induced by the main triggers of acute pancreatitis. The acinar cells were isolated from the pancreas of male Swiss mice. The cells were pre-incubated with ConA and ConBr for 1h followed by the induction of cell damage by SATC, ethanol or APO administration for 30 min (room temperature, RT). To evaluate the role of the lectin domain of ConBr and ConA, the lectins were preincubated for 1h at 37ÂC with its alpha-methyl-mannoside (α-MM) ligand sugar, or with a nonbinding sugar, D-galactose, both at a concentration of 0.2M, prior to experimental protocols. All groups were incubated for 5 minutes with the nuclear marker Hoechst 33342 (50 Âg/ml) and with the necrosis marker, propidium iodide (PI; 10 Âg/ml). In another analysis, ConA and ConBr conjugated to fluorescein isothiocyanate (FITC) were incubated for 1h (RT) with the acinar cells. To evaluate the effect of ConA and ConBr effect on mitochondrial membrane potential (ΔѰm) of pancreatic acinar cells under administration of SATC, ethanol or APO, the cells were stained with Hoechst 33342, and tetramethylrhodamine methyl ester (TMRM, fluorescent dye that is readily sequestered by active mitochondria). All analyzes were performed using confocal microscope FluoViewTM 1000 - Olympus. The results showed that the SATC, ethanol and APO groups caused significant necrosis on cells compared to control groups, and pretreatment ConBr and ConA caused a significant protection against harmful necrosis caused by all three agents. When lectins were complexed to their α-MM ligand sugar, this protective effect was significantly reversed; not being changed, however, by no specific sugar D-galactose, suggesting a participation of the lectin domain in protective effect. Lectins conjugated with FITC showed a marking on acinar cells at the level of membrane, confirming its interaction with carbohydrates present on the surface of these cells. In the analysis of mitochondrial potential, SATC, ethanol and mainly APO triggered intense depolarization of ΔѰm of pancreatic acinar cells. Pretreatment with ConA prevented mitochondrial dysfunction in all injury models, however ConBr prevented this injury caused by a dysfunction in SATC and ethanol, without changing the dysfunction caused by APO. Given the above, Con A and Con Br protect pancreatic acinar cells against necrosis induced by sulfated taurolithocholic acid, ethanol and APO with its effects mediated by lectin domain, beyond of the maintenance the integrity of the mitochondrial membrane of pancreatic cell, determinant factor to prevent the course of necrosis in acute pancreatitis. |
publishDate |
2015 |
dc.date.issued.fl_str_mv |
2015-01-19 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/masterThesis |
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publishedVersion |
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masterThesis |
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http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=13880 |
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Universidade Federal do Cearà |
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Programa de PÃs-GraduaÃÃo em Farmacologia |
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UFC |
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Universidade Federal do Cearà |
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