P2X(7) Receptor in the Kidneys of Diabetic Rats Submitted to Aerobic Training or to N-Acetylcysteine Supplementation
Autor(a) principal: | |
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Data de Publicação: | 2014 |
Outros Autores: | , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://dx.doi.org/10.1371/journal.pone.0097452 http://repositorio.unifesp.br/handle/11600/37876 |
Resumo: | Previous studies in our laboratory showed that N-acetylcysteine supplementation or aerobic training reduced oxidative stress and the progression of diabetic nephropathy in rats. the P2X(7) receptor is up-regulated in pathological conditions, such as diabetes mellitus. This up-regulation is related to oxidative stress and induces tissue apoptosis or necrosis. the aim of the present study is to assess the role of P2X(7) receptor in the kidneys of diabetic rats submitted to aerobic training or N-acetylcysteine supplementation. Diabetes was induced in male Wistar rats by streptozotocin (60 mg/kg, i.v.) and the training was done on a treadmill; N-acetylcysteine was given in the drinking water (600 mg/L). By confocal microscopy, as compared to control, the kidneys of diabetic rats showed increased P2X7 receptor expression and a higher activation in response to 2'(3')-O-(4-benzoylbenzoyl) adenosine5'-triphosphate (specific agonist) and adenosine triphosphate (nonspecific agonist) (all p<0.05). All these alterations were reduced in diabetic rats treated with N-acetylcysteine, exercise or both. We also observed measured proteinuria and albuminuria (early marker of diabetic nephropathy) in DM groups. Lipoperoxidation was strongly correlated with P2X(7) receptor expression, which was also correlated to NO center dot, thus associating this receptor to oxidative stress and kidney lesion. We suggest that P2X(7) receptor inhibition associated with the maintenance of redox homeostasis could be useful as coadjuvant treatment to delay the progression of diabetic nephropathy. |
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P2X(7) Receptor in the Kidneys of Diabetic Rats Submitted to Aerobic Training or to N-Acetylcysteine SupplementationPrevious studies in our laboratory showed that N-acetylcysteine supplementation or aerobic training reduced oxidative stress and the progression of diabetic nephropathy in rats. the P2X(7) receptor is up-regulated in pathological conditions, such as diabetes mellitus. This up-regulation is related to oxidative stress and induces tissue apoptosis or necrosis. the aim of the present study is to assess the role of P2X(7) receptor in the kidneys of diabetic rats submitted to aerobic training or N-acetylcysteine supplementation. Diabetes was induced in male Wistar rats by streptozotocin (60 mg/kg, i.v.) and the training was done on a treadmill; N-acetylcysteine was given in the drinking water (600 mg/L). By confocal microscopy, as compared to control, the kidneys of diabetic rats showed increased P2X7 receptor expression and a higher activation in response to 2'(3')-O-(4-benzoylbenzoyl) adenosine5'-triphosphate (specific agonist) and adenosine triphosphate (nonspecific agonist) (all p<0.05). All these alterations were reduced in diabetic rats treated with N-acetylcysteine, exercise or both. We also observed measured proteinuria and albuminuria (early marker of diabetic nephropathy) in DM groups. Lipoperoxidation was strongly correlated with P2X(7) receptor expression, which was also correlated to NO center dot, thus associating this receptor to oxidative stress and kidney lesion. We suggest that P2X(7) receptor inhibition associated with the maintenance of redox homeostasis could be useful as coadjuvant treatment to delay the progression of diabetic nephropathy.Universidade Federal de São Paulo, Div Nephrol, Dept Med, São Paulo, BrazilUniversidade Federal de São Paulo, Cardiovasc Div, Dept Physiol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Neurol Neurosurg, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biochem, São Paulo, BrazilUniversidade Federal de São Paulo, Div Mol Biol, Dept Biophys, São Paulo, BrazilUniversidade Federal de São Paulo, Investigat Pathol Div, Dept Pathol, São Paulo, BrazilUniversidade Federal de São Paulo, Emergency Div, Dept Med, São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, Dept Med, São Paulo, BrazilUniversidade Federal de São Paulo, Cardiovasc Div, Dept Physiol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Neurol Neurosurg, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biochem, São Paulo, BrazilUniversidade Federal de São Paulo, Div Mol Biol, Dept Biophys, São Paulo, BrazilUniversidade Federal de São Paulo, Investigat Pathol Div, Dept Pathol, São Paulo, BrazilUniversidade Federal de São Paulo, Emergency Div, Dept Med, São Paulo, BrazilWeb of ScienceFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fundacao de Apoio a Universidade Federal de São Paulo (FAP)Public Library ScienceUniversidade Federal de São Paulo (UNIFESP)Rodrigues, Adelson M. [UNIFESP]Bergamaschi, Cassia T. [UNIFESP]Fernandes, Maria Jose S. [UNIFESP]Paredes-Gamero, Edgar Julian [UNIFESP]Curi, Marcus V. [UNIFESP]Ferreira, Alice T. [UNIFESP]Araujo, Sergio R. R. [UNIFESP]Punaro, Giovana R. [UNIFESP]Maciel, Fabiane R. [UNIFESP]Nogueira, Guilherme B. [UNIFESP]Higa, Elisa Mieko Suemitsu [UNIFESP]2016-01-24T14:37:27Z2016-01-24T14:37:27Z2014-06-18info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion13application/pdfhttp://dx.doi.org/10.1371/journal.pone.0097452Plos One. San Francisco: Public Library Science, v. 9, n. 6, 13 p., 2014.10.1371/journal.pone.0097452WOS000338508200004.pdf1932-6203http://repositorio.unifesp.br/handle/11600/37876WOS:000338508200004engPlos Oneinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-08-08T11:29:22Zoai:repositorio.unifesp.br/:11600/37876Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-08-08T11:29:22Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
P2X(7) Receptor in the Kidneys of Diabetic Rats Submitted to Aerobic Training or to N-Acetylcysteine Supplementation |
title |
P2X(7) Receptor in the Kidneys of Diabetic Rats Submitted to Aerobic Training or to N-Acetylcysteine Supplementation |
spellingShingle |
P2X(7) Receptor in the Kidneys of Diabetic Rats Submitted to Aerobic Training or to N-Acetylcysteine Supplementation Rodrigues, Adelson M. [UNIFESP] |
title_short |
P2X(7) Receptor in the Kidneys of Diabetic Rats Submitted to Aerobic Training or to N-Acetylcysteine Supplementation |
title_full |
P2X(7) Receptor in the Kidneys of Diabetic Rats Submitted to Aerobic Training or to N-Acetylcysteine Supplementation |
title_fullStr |
P2X(7) Receptor in the Kidneys of Diabetic Rats Submitted to Aerobic Training or to N-Acetylcysteine Supplementation |
title_full_unstemmed |
P2X(7) Receptor in the Kidneys of Diabetic Rats Submitted to Aerobic Training or to N-Acetylcysteine Supplementation |
title_sort |
P2X(7) Receptor in the Kidneys of Diabetic Rats Submitted to Aerobic Training or to N-Acetylcysteine Supplementation |
author |
Rodrigues, Adelson M. [UNIFESP] |
author_facet |
Rodrigues, Adelson M. [UNIFESP] Bergamaschi, Cassia T. [UNIFESP] Fernandes, Maria Jose S. [UNIFESP] Paredes-Gamero, Edgar Julian [UNIFESP] Curi, Marcus V. [UNIFESP] Ferreira, Alice T. [UNIFESP] Araujo, Sergio R. R. [UNIFESP] Punaro, Giovana R. [UNIFESP] Maciel, Fabiane R. [UNIFESP] Nogueira, Guilherme B. [UNIFESP] Higa, Elisa Mieko Suemitsu [UNIFESP] |
author_role |
author |
author2 |
Bergamaschi, Cassia T. [UNIFESP] Fernandes, Maria Jose S. [UNIFESP] Paredes-Gamero, Edgar Julian [UNIFESP] Curi, Marcus V. [UNIFESP] Ferreira, Alice T. [UNIFESP] Araujo, Sergio R. R. [UNIFESP] Punaro, Giovana R. [UNIFESP] Maciel, Fabiane R. [UNIFESP] Nogueira, Guilherme B. [UNIFESP] Higa, Elisa Mieko Suemitsu [UNIFESP] |
author2_role |
author author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Rodrigues, Adelson M. [UNIFESP] Bergamaschi, Cassia T. [UNIFESP] Fernandes, Maria Jose S. [UNIFESP] Paredes-Gamero, Edgar Julian [UNIFESP] Curi, Marcus V. [UNIFESP] Ferreira, Alice T. [UNIFESP] Araujo, Sergio R. R. [UNIFESP] Punaro, Giovana R. [UNIFESP] Maciel, Fabiane R. [UNIFESP] Nogueira, Guilherme B. [UNIFESP] Higa, Elisa Mieko Suemitsu [UNIFESP] |
description |
Previous studies in our laboratory showed that N-acetylcysteine supplementation or aerobic training reduced oxidative stress and the progression of diabetic nephropathy in rats. the P2X(7) receptor is up-regulated in pathological conditions, such as diabetes mellitus. This up-regulation is related to oxidative stress and induces tissue apoptosis or necrosis. the aim of the present study is to assess the role of P2X(7) receptor in the kidneys of diabetic rats submitted to aerobic training or N-acetylcysteine supplementation. Diabetes was induced in male Wistar rats by streptozotocin (60 mg/kg, i.v.) and the training was done on a treadmill; N-acetylcysteine was given in the drinking water (600 mg/L). By confocal microscopy, as compared to control, the kidneys of diabetic rats showed increased P2X7 receptor expression and a higher activation in response to 2'(3')-O-(4-benzoylbenzoyl) adenosine5'-triphosphate (specific agonist) and adenosine triphosphate (nonspecific agonist) (all p<0.05). All these alterations were reduced in diabetic rats treated with N-acetylcysteine, exercise or both. We also observed measured proteinuria and albuminuria (early marker of diabetic nephropathy) in DM groups. Lipoperoxidation was strongly correlated with P2X(7) receptor expression, which was also correlated to NO center dot, thus associating this receptor to oxidative stress and kidney lesion. We suggest that P2X(7) receptor inhibition associated with the maintenance of redox homeostasis could be useful as coadjuvant treatment to delay the progression of diabetic nephropathy. |
publishDate |
2014 |
dc.date.none.fl_str_mv |
2014-06-18 2016-01-24T14:37:27Z 2016-01-24T14:37:27Z |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1371/journal.pone.0097452 Plos One. San Francisco: Public Library Science, v. 9, n. 6, 13 p., 2014. 10.1371/journal.pone.0097452 WOS000338508200004.pdf 1932-6203 http://repositorio.unifesp.br/handle/11600/37876 WOS:000338508200004 |
url |
http://dx.doi.org/10.1371/journal.pone.0097452 http://repositorio.unifesp.br/handle/11600/37876 |
identifier_str_mv |
Plos One. San Francisco: Public Library Science, v. 9, n. 6, 13 p., 2014. 10.1371/journal.pone.0097452 WOS000338508200004.pdf 1932-6203 WOS:000338508200004 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Plos One |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
13 application/pdf |
dc.publisher.none.fl_str_mv |
Public Library Science |
publisher.none.fl_str_mv |
Public Library Science |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
biblioteca.csp@unifesp.br |
_version_ |
1814268350841225216 |