Chalcones isolated from myracrodruon urundeuva and 2-methyl-inositol isolated from Magonia glabrata protect neurons from 6-hydroxydopamine-induced oxidative injury and apoptose: study in rat mesencephalic cell cultures
Autor(a) principal: | |
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Data de Publicação: | 2005 |
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=7 |
Resumo: | The present work evaluated the cytoprotective effect of chalcone-enriched fraction (CEF) and 2-methyl-inositol (MIT) in primary rat mesencephalic cell culture exposed to the neurotoxin 6-hydroxydopamine (6-OHDA). The CEF was obtained from Myracrodruon urundeuva, a Brazilian medicinal plant used as an antiinflamatory and wound healing agent.in female genital tract. In this fraction there are the dimerics chalcones urundeuvinas A, B e C The other compound was the MIT isolated from Magonia glabrata, a plant popularly known as âTingui de Bolaâ, which bark from its root is used as poison to catch the fishes from lakes and rivers. The immunohistochemical assay for tyrosine hydroxylase revealed that the percentage of dopaminergic cells in our cultures is approximately 2%. After exposition to 6-OHDA (40 and 200 microM) the cellular viability was reduced to 88,81% and 35,45% respectively. The mitochondrial activity was reduced to 88,8 and 35,4%, the nitrite levels was increased to 551,9% and 721,3% respectively and the lipid peroxidation was increased to 166,84% in the concentration of 200 microM, as observed in the MTT, nitrite and TBARS assays respectively. The results show that the exposition to CEF (100 microg/mL) before 6-OHDA (neuroprevention experiment) or after 6-OHDA (neurorescue experiment) reduced significantly the cell death caused by 6-OHDA (40 e 200 microM). The CEF prevented significantly the increase in nitrite levels induced by 6-OHDA (40 and 200 microM) (in both experiments), except in the neurorescue experiment in which the CEF failed to revert the increase in nitrite levels generated by 6-OHDA (200 microM). The CEF inhibited the lipid peroxidation induced by 6-OHDA (200 microM) in both experiments, and also showed antiapoptotic activity against 6-OHDA (40 and 200 microM) in both experiments. The MIT protected significantly TH- and TH+ cells from injury induced by 6-OHDA (40 and 200 microM) in both experiments. It showed a reduction in the nitrite levels generated by 6-OHDA in both experiments. The MIT also reverted the lipid peroxidation generated by 6-OHDA (200 microM) and showed antiapoptotic activity against 6-OHDA (40 and 200 microM) in both experiments. These results suggest that the neuroprotective action these compounds, CEF and MIT are due to antioxidant, besides a possible mitochondrial protection of these polyphenols. In related to MIT not must be discarded the idea of a second messenger action through the production of inositol triphosphate and protein kinase C activation. The findings may have a clinical importance in neurodegenerative conditions like Parkinsonâs disease |
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info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/doctoralThesisChalcones isolated from myracrodruon urundeuva and 2-methyl-inositol isolated from Magonia glabrata protect neurons from 6-hydroxydopamine-induced oxidative injury and apoptose: study in rat mesencephalic cell culturesChalconas isoladas da myracrodruon urundeuva e 2-O-metilinositol isolado da magonia glabrata protegem neurÃnios de danos oxidativos e apoptose induzida por 6-hidroxidopamina (6-OHDA): estudo em cultura primÃria de cÃlulas mesencefÃlicas de ratos2005-08-11Geanne Matos de Andrade21911258320http://lattes.cnpq.br/9935129797137635Manoel Odorico de Moraes Filho04854543353http://lattes.cnpq.br/0701679734111287John Fontenele AraÃjo22800662387http://lattes.cnpq.br/3347815035685882Maria das GraÃas Naffah Mazzacoratti01218274883http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4783016J476433102387http://lattes.cnpq.br/3748078587451434HÃlio Vitoriano Nobre JÃniorUniversidade Federal do CearÃPrograma de PÃs-GraduaÃÃo em FarmacologiaUFCBRCulturas de CÃlula MesencefÃlicas 6-hidroxidopamina PeroxidaÃÃo LipÃdicaNeuroprevenÃÃoNeuroresgate Myracrodruoun urundeuva Magonia glabrata Chalconas Urundeuvinas 2-O-metilinositolMesencephalic Cell Culture 6-hydroxydopamine Lipid Peroxidation Neuroprevention Neurorescue Myracrodruoun urundeuva Magonia glabrata Chalcone-enriched fraction Urundeuvine 2-O-metilinositolFARMACOLOGIAThe present work evaluated the cytoprotective effect of chalcone-enriched fraction (CEF) and 2-methyl-inositol (MIT) in primary rat mesencephalic cell culture exposed to the neurotoxin 6-hydroxydopamine (6-OHDA). The CEF was obtained from Myracrodruon urundeuva, a Brazilian medicinal plant used as an antiinflamatory and wound healing agent.in female genital tract. In this fraction there are the dimerics chalcones urundeuvinas A, B e C The other compound was the MIT isolated from Magonia glabrata, a plant popularly known as âTingui de Bolaâ, which bark from its root is used as poison to catch the fishes from lakes and rivers. The immunohistochemical assay for tyrosine hydroxylase revealed that the percentage of dopaminergic cells in our cultures is approximately 2%. After exposition to 6-OHDA (40 and 200 microM) the cellular viability was reduced to 88,81% and 35,45% respectively. The mitochondrial activity was reduced to 88,8 and 35,4%, the nitrite levels was increased to 551,9% and 721,3% respectively and the lipid peroxidation was increased to 166,84% in the concentration of 200 microM, as observed in the MTT, nitrite and TBARS assays respectively. The results show that the exposition to CEF (100 microg/mL) before 6-OHDA (neuroprevention experiment) or after 6-OHDA (neurorescue experiment) reduced significantly the cell death caused by 6-OHDA (40 e 200 microM). The CEF prevented significantly the increase in nitrite levels induced by 6-OHDA (40 and 200 microM) (in both experiments), except in the neurorescue experiment in which the CEF failed to revert the increase in nitrite levels generated by 6-OHDA (200 microM). The CEF inhibited the lipid peroxidation induced by 6-OHDA (200 microM) in both experiments, and also showed antiapoptotic activity against 6-OHDA (40 and 200 microM) in both experiments. The MIT protected significantly TH- and TH+ cells from injury induced by 6-OHDA (40 and 200 microM) in both experiments. It showed a reduction in the nitrite levels generated by 6-OHDA in both experiments. The MIT also reverted the lipid peroxidation generated by 6-OHDA (200 microM) and showed antiapoptotic activity against 6-OHDA (40 and 200 microM) in both experiments. These results suggest that the neuroprotective action these compounds, CEF and MIT are due to antioxidant, besides a possible mitochondrial protection of these polyphenols. In related to MIT not must be discarded the idea of a second messenger action through the production of inositol triphosphate and protein kinase C activation. The findings may have a clinical importance in neurodegenerative conditions like Parkinsonâs diseaseNo presente trabalho, estudou-se o efeito citoprotetor da fraÃÃo enriquecida de chalconas (FEC) e do 2-O-metilinositol (MIT) em cultura primÃria de cÃlulas mesencefÃlicas de ratos expostas à neurotoxina 6-hidroxidopamina (6-OHDA). A FEC foi isolada de Myracrodruoun urundeuva, planta medicinal brasileira comumente utilizada como antiinflamatÃrio do trato genital feminino. Nesta fraÃÃo estÃo presentes as chalconas dimÃricas urundeuvinas A, B e C. Outro composto estudado foi o MIT, isolado de Magonia glabrata, uma planta popularmente conhecida como âTingui de Bolaâ, cujas cascas de suas raÃzes sÃo usadas como âvenenoâ para facilitar a pesca nos lagos e rios. O MIT à um monossacarideo com um Ãnico anel da estrutura poli-hidroxilada. Apesar de relatos da toxicidade desta planta, o composto estudado nÃo apresentou toxicidade. As cÃlulas foram cultivadas durante quatro dias e apÃs este tempo foram prÃ-incubadas com FEC ou MIT trÃs horas antes (Protocolo de neuroprevenÃÃo) ou trÃs horas apÃs (Protocolo de neuroresgate) a adiÃÃo da 6-OHDA. A imunohistoquÃmica para tirosina hidroxilase revelou um percentual de cÃlulas dopaminÃrgicas em torno de 2%. A 6-OHDA (40 e 200 microM), promoveu uma diminuiÃÃo na viabilidade celular em torno de 37,65% e 63,44% para cÃlulas nÃo dopaminÃrgicas (TH-) e (79,78% e 93,75%) para cÃlulas dopaminÃrgicas (TH+) e aumentou os nÃveis de nitrito para 551,9% e 721,3% respectivamente em relaÃÃo ao controle. AlÃm disso induziu uma grande peroxidaÃÃo lipÃdica (aumento de 166,84%) como observados pelos ensaios MTT, nitrito e TBARS, respectivamente. Na concentraÃÃo de 200microM a 6-OHDA induziu uma grande morte celular, com aumento de cÃlulas em apoptose tardia e necrose. Os resultados mostraram que a FEC (1; 10 e 100 microg/mL) reduziu significativamente e de maneira dose-dependente (p menor igual a0,05) a morte celular induzida pela 6-OHDA (40 e 200 microM). AlÃm disso preveniu o aumento de nitrito e a peroxidaÃÃo lipÃdica. A FEC demonstrou atividade antiapoptÃtica e preveniu a necrose causada pela 6-OHDA (200 microM) (nos dois Protocolos estudados). O MIT (1, 10 e 100 microg/mL) protegeu tanto as cÃlulas TH- quanto TH+ do dano induzido pela 6-OHDA (40 e 200microM) (em ambos os Protocolos), reduzindo os nÃveis de nitrito e a peroxidaÃÃo lÃpidica. TambÃm demonstrou uma potente atividade antiapoptÃtica. Estes resultados demonstram que a neuroproteÃÃo dos compostos estudados, FEC e MIT, se deva as aÃÃes antioxidante, alÃm de uma proteÃÃo a nÃvel mitocondrial destes polifenois, no caso do MIT tambÃm nÃo se podendo descartar uma aÃÃo a nÃvel de segundo mensageiro, via formaÃÃo de inositol trifosfato e ativaÃÃo de PKC. Os achados podem ter uma futura importÃncia clÃnica em doenÃas neurodegenerativas tais como na DoenÃa de ParkinsonCoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superiorhttp://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=7application/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.en.fl_str_mv |
Chalcones isolated from myracrodruon urundeuva and 2-methyl-inositol isolated from Magonia glabrata protect neurons from 6-hydroxydopamine-induced oxidative injury and apoptose: study in rat mesencephalic cell cultures |
dc.title.alternative.pt.fl_str_mv |
Chalconas isoladas da myracrodruon urundeuva e 2-O-metilinositol isolado da magonia glabrata protegem neurÃnios de danos oxidativos e apoptose induzida por 6-hidroxidopamina (6-OHDA): estudo em cultura primÃria de cÃlulas mesencefÃlicas de ratos |
title |
Chalcones isolated from myracrodruon urundeuva and 2-methyl-inositol isolated from Magonia glabrata protect neurons from 6-hydroxydopamine-induced oxidative injury and apoptose: study in rat mesencephalic cell cultures |
spellingShingle |
Chalcones isolated from myracrodruon urundeuva and 2-methyl-inositol isolated from Magonia glabrata protect neurons from 6-hydroxydopamine-induced oxidative injury and apoptose: study in rat mesencephalic cell cultures HÃlio Vitoriano Nobre JÃnior Culturas de CÃlula MesencefÃlicas 6-hidroxidopamina PeroxidaÃÃo LipÃdica NeuroprevenÃÃo Neuroresgate Myracrodruoun urundeuva Magonia glabrata Chalconas Urundeuvinas 2-O-metilinositol Mesencephalic Cell Culture 6-hydroxydopamine Lipid Peroxidation Neuroprevention Neurorescue Myracrodruoun urundeuva Magonia glabrata Chalcone-enriched fraction Urundeuvine 2-O-metilinositol FARMACOLOGIA |
title_short |
Chalcones isolated from myracrodruon urundeuva and 2-methyl-inositol isolated from Magonia glabrata protect neurons from 6-hydroxydopamine-induced oxidative injury and apoptose: study in rat mesencephalic cell cultures |
title_full |
Chalcones isolated from myracrodruon urundeuva and 2-methyl-inositol isolated from Magonia glabrata protect neurons from 6-hydroxydopamine-induced oxidative injury and apoptose: study in rat mesencephalic cell cultures |
title_fullStr |
Chalcones isolated from myracrodruon urundeuva and 2-methyl-inositol isolated from Magonia glabrata protect neurons from 6-hydroxydopamine-induced oxidative injury and apoptose: study in rat mesencephalic cell cultures |
title_full_unstemmed |
Chalcones isolated from myracrodruon urundeuva and 2-methyl-inositol isolated from Magonia glabrata protect neurons from 6-hydroxydopamine-induced oxidative injury and apoptose: study in rat mesencephalic cell cultures |
title_sort |
Chalcones isolated from myracrodruon urundeuva and 2-methyl-inositol isolated from Magonia glabrata protect neurons from 6-hydroxydopamine-induced oxidative injury and apoptose: study in rat mesencephalic cell cultures |
author |
HÃlio Vitoriano Nobre JÃnior |
author_facet |
HÃlio Vitoriano Nobre JÃnior |
author_role |
author |
dc.contributor.advisor1.fl_str_mv |
Geanne Matos de Andrade |
dc.contributor.advisor1ID.fl_str_mv |
21911258320 |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/9935129797137635 |
dc.contributor.referee1.fl_str_mv |
Manoel Odorico de Moraes Filho |
dc.contributor.referee1ID.fl_str_mv |
04854543353 |
dc.contributor.referee1Lattes.fl_str_mv |
http://lattes.cnpq.br/0701679734111287 |
dc.contributor.referee2.fl_str_mv |
John Fontenele AraÃjo |
dc.contributor.referee2ID.fl_str_mv |
22800662387 |
dc.contributor.referee2Lattes.fl_str_mv |
http://lattes.cnpq.br/3347815035685882 |
dc.contributor.referee3.fl_str_mv |
Maria das GraÃas Naffah Mazzacoratti |
dc.contributor.referee3ID.fl_str_mv |
01218274883 |
dc.contributor.referee3Lattes.fl_str_mv |
http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4783016J4 |
dc.contributor.authorID.fl_str_mv |
76433102387 |
dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/3748078587451434 |
dc.contributor.author.fl_str_mv |
HÃlio Vitoriano Nobre JÃnior |
contributor_str_mv |
Geanne Matos de Andrade Manoel Odorico de Moraes Filho John Fontenele AraÃjo Maria das GraÃas Naffah Mazzacoratti |
dc.subject.por.fl_str_mv |
Culturas de CÃlula MesencefÃlicas 6-hidroxidopamina PeroxidaÃÃo LipÃdica NeuroprevenÃÃo Neuroresgate Myracrodruoun urundeuva Magonia glabrata Chalconas Urundeuvinas 2-O-metilinositol |
topic |
Culturas de CÃlula MesencefÃlicas 6-hidroxidopamina PeroxidaÃÃo LipÃdica NeuroprevenÃÃo Neuroresgate Myracrodruoun urundeuva Magonia glabrata Chalconas Urundeuvinas 2-O-metilinositol Mesencephalic Cell Culture 6-hydroxydopamine Lipid Peroxidation Neuroprevention Neurorescue Myracrodruoun urundeuva Magonia glabrata Chalcone-enriched fraction Urundeuvine 2-O-metilinositol FARMACOLOGIA |
dc.subject.eng.fl_str_mv |
Mesencephalic Cell Culture 6-hydroxydopamine Lipid Peroxidation Neuroprevention Neurorescue Myracrodruoun urundeuva Magonia glabrata Chalcone-enriched fraction Urundeuvine 2-O-metilinositol |
dc.subject.cnpq.fl_str_mv |
FARMACOLOGIA |
dc.description.sponsorship.fl_txt_mv |
CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior |
dc.description.abstract.por.fl_txt_mv |
The present work evaluated the cytoprotective effect of chalcone-enriched fraction (CEF) and 2-methyl-inositol (MIT) in primary rat mesencephalic cell culture exposed to the neurotoxin 6-hydroxydopamine (6-OHDA). The CEF was obtained from Myracrodruon urundeuva, a Brazilian medicinal plant used as an antiinflamatory and wound healing agent.in female genital tract. In this fraction there are the dimerics chalcones urundeuvinas A, B e C The other compound was the MIT isolated from Magonia glabrata, a plant popularly known as âTingui de Bolaâ, which bark from its root is used as poison to catch the fishes from lakes and rivers. The immunohistochemical assay for tyrosine hydroxylase revealed that the percentage of dopaminergic cells in our cultures is approximately 2%. After exposition to 6-OHDA (40 and 200 microM) the cellular viability was reduced to 88,81% and 35,45% respectively. The mitochondrial activity was reduced to 88,8 and 35,4%, the nitrite levels was increased to 551,9% and 721,3% respectively and the lipid peroxidation was increased to 166,84% in the concentration of 200 microM, as observed in the MTT, nitrite and TBARS assays respectively. The results show that the exposition to CEF (100 microg/mL) before 6-OHDA (neuroprevention experiment) or after 6-OHDA (neurorescue experiment) reduced significantly the cell death caused by 6-OHDA (40 e 200 microM). The CEF prevented significantly the increase in nitrite levels induced by 6-OHDA (40 and 200 microM) (in both experiments), except in the neurorescue experiment in which the CEF failed to revert the increase in nitrite levels generated by 6-OHDA (200 microM). The CEF inhibited the lipid peroxidation induced by 6-OHDA (200 microM) in both experiments, and also showed antiapoptotic activity against 6-OHDA (40 and 200 microM) in both experiments. The MIT protected significantly TH- and TH+ cells from injury induced by 6-OHDA (40 and 200 microM) in both experiments. It showed a reduction in the nitrite levels generated by 6-OHDA in both experiments. The MIT also reverted the lipid peroxidation generated by 6-OHDA (200 microM) and showed antiapoptotic activity against 6-OHDA (40 and 200 microM) in both experiments. These results suggest that the neuroprotective action these compounds, CEF and MIT are due to antioxidant, besides a possible mitochondrial protection of these polyphenols. In related to MIT not must be discarded the idea of a second messenger action through the production of inositol triphosphate and protein kinase C activation. The findings may have a clinical importance in neurodegenerative conditions like Parkinsonâs disease No presente trabalho, estudou-se o efeito citoprotetor da fraÃÃo enriquecida de chalconas (FEC) e do 2-O-metilinositol (MIT) em cultura primÃria de cÃlulas mesencefÃlicas de ratos expostas à neurotoxina 6-hidroxidopamina (6-OHDA). A FEC foi isolada de Myracrodruoun urundeuva, planta medicinal brasileira comumente utilizada como antiinflamatÃrio do trato genital feminino. Nesta fraÃÃo estÃo presentes as chalconas dimÃricas urundeuvinas A, B e C. Outro composto estudado foi o MIT, isolado de Magonia glabrata, uma planta popularmente conhecida como âTingui de Bolaâ, cujas cascas de suas raÃzes sÃo usadas como âvenenoâ para facilitar a pesca nos lagos e rios. O MIT à um monossacarideo com um Ãnico anel da estrutura poli-hidroxilada. Apesar de relatos da toxicidade desta planta, o composto estudado nÃo apresentou toxicidade. As cÃlulas foram cultivadas durante quatro dias e apÃs este tempo foram prÃ-incubadas com FEC ou MIT trÃs horas antes (Protocolo de neuroprevenÃÃo) ou trÃs horas apÃs (Protocolo de neuroresgate) a adiÃÃo da 6-OHDA. A imunohistoquÃmica para tirosina hidroxilase revelou um percentual de cÃlulas dopaminÃrgicas em torno de 2%. A 6-OHDA (40 e 200 microM), promoveu uma diminuiÃÃo na viabilidade celular em torno de 37,65% e 63,44% para cÃlulas nÃo dopaminÃrgicas (TH-) e (79,78% e 93,75%) para cÃlulas dopaminÃrgicas (TH+) e aumentou os nÃveis de nitrito para 551,9% e 721,3% respectivamente em relaÃÃo ao controle. AlÃm disso induziu uma grande peroxidaÃÃo lipÃdica (aumento de 166,84%) como observados pelos ensaios MTT, nitrito e TBARS, respectivamente. Na concentraÃÃo de 200microM a 6-OHDA induziu uma grande morte celular, com aumento de cÃlulas em apoptose tardia e necrose. Os resultados mostraram que a FEC (1; 10 e 100 microg/mL) reduziu significativamente e de maneira dose-dependente (p menor igual a0,05) a morte celular induzida pela 6-OHDA (40 e 200 microM). AlÃm disso preveniu o aumento de nitrito e a peroxidaÃÃo lipÃdica. A FEC demonstrou atividade antiapoptÃtica e preveniu a necrose causada pela 6-OHDA (200 microM) (nos dois Protocolos estudados). O MIT (1, 10 e 100 microg/mL) protegeu tanto as cÃlulas TH- quanto TH+ do dano induzido pela 6-OHDA (40 e 200microM) (em ambos os Protocolos), reduzindo os nÃveis de nitrito e a peroxidaÃÃo lÃpidica. TambÃm demonstrou uma potente atividade antiapoptÃtica. Estes resultados demonstram que a neuroproteÃÃo dos compostos estudados, FEC e MIT, se deva as aÃÃes antioxidante, alÃm de uma proteÃÃo a nÃvel mitocondrial destes polifenois, no caso do MIT tambÃm nÃo se podendo descartar uma aÃÃo a nÃvel de segundo mensageiro, via formaÃÃo de inositol trifosfato e ativaÃÃo de PKC. Os achados podem ter uma futura importÃncia clÃnica em doenÃas neurodegenerativas tais como na DoenÃa de Parkinson |
description |
The present work evaluated the cytoprotective effect of chalcone-enriched fraction (CEF) and 2-methyl-inositol (MIT) in primary rat mesencephalic cell culture exposed to the neurotoxin 6-hydroxydopamine (6-OHDA). The CEF was obtained from Myracrodruon urundeuva, a Brazilian medicinal plant used as an antiinflamatory and wound healing agent.in female genital tract. In this fraction there are the dimerics chalcones urundeuvinas A, B e C The other compound was the MIT isolated from Magonia glabrata, a plant popularly known as âTingui de Bolaâ, which bark from its root is used as poison to catch the fishes from lakes and rivers. The immunohistochemical assay for tyrosine hydroxylase revealed that the percentage of dopaminergic cells in our cultures is approximately 2%. After exposition to 6-OHDA (40 and 200 microM) the cellular viability was reduced to 88,81% and 35,45% respectively. The mitochondrial activity was reduced to 88,8 and 35,4%, the nitrite levels was increased to 551,9% and 721,3% respectively and the lipid peroxidation was increased to 166,84% in the concentration of 200 microM, as observed in the MTT, nitrite and TBARS assays respectively. The results show that the exposition to CEF (100 microg/mL) before 6-OHDA (neuroprevention experiment) or after 6-OHDA (neurorescue experiment) reduced significantly the cell death caused by 6-OHDA (40 e 200 microM). The CEF prevented significantly the increase in nitrite levels induced by 6-OHDA (40 and 200 microM) (in both experiments), except in the neurorescue experiment in which the CEF failed to revert the increase in nitrite levels generated by 6-OHDA (200 microM). The CEF inhibited the lipid peroxidation induced by 6-OHDA (200 microM) in both experiments, and also showed antiapoptotic activity against 6-OHDA (40 and 200 microM) in both experiments. The MIT protected significantly TH- and TH+ cells from injury induced by 6-OHDA (40 and 200 microM) in both experiments. It showed a reduction in the nitrite levels generated by 6-OHDA in both experiments. The MIT also reverted the lipid peroxidation generated by 6-OHDA (200 microM) and showed antiapoptotic activity against 6-OHDA (40 and 200 microM) in both experiments. These results suggest that the neuroprotective action these compounds, CEF and MIT are due to antioxidant, besides a possible mitochondrial protection of these polyphenols. In related to MIT not must be discarded the idea of a second messenger action through the production of inositol triphosphate and protein kinase C activation. The findings may have a clinical importance in neurodegenerative conditions like Parkinsonâs disease |
publishDate |
2005 |
dc.date.issued.fl_str_mv |
2005-08-11 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/doctoralThesis |
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doctoralThesis |
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http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=7 |
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Universidade Federal do Cearà |
dc.publisher.program.fl_str_mv |
Programa de PÃs-GraduaÃÃo em Farmacologia |
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UFC |
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BR |
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Universidade Federal do Cearà |
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