Oleanolic acid: a promising neuroprotective agent for cerebral ischemia

Autores
Caltana, Laura Romina; Nieto, Maria Luisa; Brusco, Herminia Alicia
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Stroke is considered the most common and severely disabling neurologicaldisease. It is one of the leading causes of death after heartdisease and cancer, causing 10% deaths worldwide and involvingrisk factors such as smoking, obesity and nutritional disbalance.Disability affects 75% of stroke survivors through severe mentaland/or physical impairment depending on the affected brain area(Go et al., 2014).Stroke treatment is limited to thrombolysis and antiplatelettherapy with a tissue plasminogen activator (tPA), which is onlyuseful if administered within 3 hours of the appearance of earlysymptoms. This therapy is only used in 1?2% stroke patients andhas, indeed, limited clinical success, as it does not protect neuronsfrom the hypoxic insult. Therefore, the development and evaluationof new drugs to reduce the life-threatening effects of strokeand hypoxia might prove extremely fruitful.Stroke is produced by a decrease in blood supply due to differenttypes of alterations in the brain blood vessels, which cause cerebralhypoxia/ischemia. In turn, the hypoxic damage produces severalchanges in gene expression patterns in brain tissue cells (neuronsand glial cells). Rapid thrombolysis is effective in protecting theinjured ischemic core, although preventing the pathological featuresthat produce neuronal death requires the development of newtreatments and the implementation of a dual therapy combiningthe disruption of the clot and the preservation of neuronal function.In this respect, many preclinical studies have been successfulin finding neuroprotective agents, but subsequent clinical trialshave rendered disappointing results.Inflammation is one of the distinctive events in stroke, whilemicroglial cells are the predominant inflammatory effectors inbrain. Reactive astrocytosis and the formation of a glial scar in theboundary zone of the ischemic core are also critical events whichcan produce both positive and negative consequences.
Fil: Caltana, Laura Romina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
Fil: Nieto, Maria Luisa. Consejo Superior de Investigaciones Científicas; España
Fil: Brusco, Herminia Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
Materia
OLEANOIC ACID
NEUROPROTECTION
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/102697

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spelling Oleanolic acid: a promising neuroprotective agent for cerebral ischemiaCaltana, Laura RominaNieto, Maria LuisaBrusco, Herminia AliciaOLEANOIC ACIDNEUROPROTECTIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Stroke is considered the most common and severely disabling neurologicaldisease. It is one of the leading causes of death after heartdisease and cancer, causing 10% deaths worldwide and involvingrisk factors such as smoking, obesity and nutritional disbalance.Disability affects 75% of stroke survivors through severe mentaland/or physical impairment depending on the affected brain area(Go et al., 2014).Stroke treatment is limited to thrombolysis and antiplatelettherapy with a tissue plasminogen activator (tPA), which is onlyuseful if administered within 3 hours of the appearance of earlysymptoms. This therapy is only used in 1?2% stroke patients andhas, indeed, limited clinical success, as it does not protect neuronsfrom the hypoxic insult. Therefore, the development and evaluationof new drugs to reduce the life-threatening effects of strokeand hypoxia might prove extremely fruitful.Stroke is produced by a decrease in blood supply due to differenttypes of alterations in the brain blood vessels, which cause cerebralhypoxia/ischemia. In turn, the hypoxic damage produces severalchanges in gene expression patterns in brain tissue cells (neuronsand glial cells). Rapid thrombolysis is effective in protecting theinjured ischemic core, although preventing the pathological featuresthat produce neuronal death requires the development of newtreatments and the implementation of a dual therapy combiningthe disruption of the clot and the preservation of neuronal function.In this respect, many preclinical studies have been successfulin finding neuroprotective agents, but subsequent clinical trialshave rendered disappointing results.Inflammation is one of the distinctive events in stroke, whilemicroglial cells are the predominant inflammatory effectors inbrain. Reactive astrocytosis and the formation of a glial scar in theboundary zone of the ischemic core are also critical events whichcan produce both positive and negative consequences.Fil: Caltana, Laura Romina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; ArgentinaFil: Nieto, Maria Luisa. Consejo Superior de Investigaciones Científicas; EspañaFil: Brusco, Herminia Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; ArgentinaShenyang Editorial Dept Neural Regeneration Res2015-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/102697Caltana, Laura Romina; Nieto, Maria Luisa; Brusco, Herminia Alicia; Oleanolic acid: a promising neuroprotective agent for cerebral ischemia; Shenyang Editorial Dept Neural Regeneration Res; Neural Regeneration Research; 10; 4; 4-2015; 540-5411673-5374CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.4103/1673-5374.155414info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424737/info:eu-repo/semantics/altIdentifier/url/http://www.nrronline.org/article.asp?issn=1673-5374;year=2015;volume=10;issue=4;spage=540;epage=541;aulast=Laurainfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:22:16Zoai:ri.conicet.gov.ar:11336/102697instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-15 15:22:17.007CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Oleanolic acid: a promising neuroprotective agent for cerebral ischemia
title Oleanolic acid: a promising neuroprotective agent for cerebral ischemia
spellingShingle Oleanolic acid: a promising neuroprotective agent for cerebral ischemia
Caltana, Laura Romina
OLEANOIC ACID
NEUROPROTECTION
title_short Oleanolic acid: a promising neuroprotective agent for cerebral ischemia
title_full Oleanolic acid: a promising neuroprotective agent for cerebral ischemia
title_fullStr Oleanolic acid: a promising neuroprotective agent for cerebral ischemia
title_full_unstemmed Oleanolic acid: a promising neuroprotective agent for cerebral ischemia
title_sort Oleanolic acid: a promising neuroprotective agent for cerebral ischemia
dc.creator.none.fl_str_mv Caltana, Laura Romina
Nieto, Maria Luisa
Brusco, Herminia Alicia
author Caltana, Laura Romina
author_facet Caltana, Laura Romina
Nieto, Maria Luisa
Brusco, Herminia Alicia
author_role author
author2 Nieto, Maria Luisa
Brusco, Herminia Alicia
author2_role author
author
dc.subject.none.fl_str_mv OLEANOIC ACID
NEUROPROTECTION
topic OLEANOIC ACID
NEUROPROTECTION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Stroke is considered the most common and severely disabling neurologicaldisease. It is one of the leading causes of death after heartdisease and cancer, causing 10% deaths worldwide and involvingrisk factors such as smoking, obesity and nutritional disbalance.Disability affects 75% of stroke survivors through severe mentaland/or physical impairment depending on the affected brain area(Go et al., 2014).Stroke treatment is limited to thrombolysis and antiplatelettherapy with a tissue plasminogen activator (tPA), which is onlyuseful if administered within 3 hours of the appearance of earlysymptoms. This therapy is only used in 1?2% stroke patients andhas, indeed, limited clinical success, as it does not protect neuronsfrom the hypoxic insult. Therefore, the development and evaluationof new drugs to reduce the life-threatening effects of strokeand hypoxia might prove extremely fruitful.Stroke is produced by a decrease in blood supply due to differenttypes of alterations in the brain blood vessels, which cause cerebralhypoxia/ischemia. In turn, the hypoxic damage produces severalchanges in gene expression patterns in brain tissue cells (neuronsand glial cells). Rapid thrombolysis is effective in protecting theinjured ischemic core, although preventing the pathological featuresthat produce neuronal death requires the development of newtreatments and the implementation of a dual therapy combiningthe disruption of the clot and the preservation of neuronal function.In this respect, many preclinical studies have been successfulin finding neuroprotective agents, but subsequent clinical trialshave rendered disappointing results.Inflammation is one of the distinctive events in stroke, whilemicroglial cells are the predominant inflammatory effectors inbrain. Reactive astrocytosis and the formation of a glial scar in theboundary zone of the ischemic core are also critical events whichcan produce both positive and negative consequences.
Fil: Caltana, Laura Romina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
Fil: Nieto, Maria Luisa. Consejo Superior de Investigaciones Científicas; España
Fil: Brusco, Herminia Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina
description Stroke is considered the most common and severely disabling neurologicaldisease. It is one of the leading causes of death after heartdisease and cancer, causing 10% deaths worldwide and involvingrisk factors such as smoking, obesity and nutritional disbalance.Disability affects 75% of stroke survivors through severe mentaland/or physical impairment depending on the affected brain area(Go et al., 2014).Stroke treatment is limited to thrombolysis and antiplatelettherapy with a tissue plasminogen activator (tPA), which is onlyuseful if administered within 3 hours of the appearance of earlysymptoms. This therapy is only used in 1?2% stroke patients andhas, indeed, limited clinical success, as it does not protect neuronsfrom the hypoxic insult. Therefore, the development and evaluationof new drugs to reduce the life-threatening effects of strokeand hypoxia might prove extremely fruitful.Stroke is produced by a decrease in blood supply due to differenttypes of alterations in the brain blood vessels, which cause cerebralhypoxia/ischemia. In turn, the hypoxic damage produces severalchanges in gene expression patterns in brain tissue cells (neuronsand glial cells). Rapid thrombolysis is effective in protecting theinjured ischemic core, although preventing the pathological featuresthat produce neuronal death requires the development of newtreatments and the implementation of a dual therapy combiningthe disruption of the clot and the preservation of neuronal function.In this respect, many preclinical studies have been successfulin finding neuroprotective agents, but subsequent clinical trialshave rendered disappointing results.Inflammation is one of the distinctive events in stroke, whilemicroglial cells are the predominant inflammatory effectors inbrain. Reactive astrocytosis and the formation of a glial scar in theboundary zone of the ischemic core are also critical events whichcan produce both positive and negative consequences.
publishDate 2015
dc.date.none.fl_str_mv 2015-04
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/102697
Caltana, Laura Romina; Nieto, Maria Luisa; Brusco, Herminia Alicia; Oleanolic acid: a promising neuroprotective agent for cerebral ischemia; Shenyang Editorial Dept Neural Regeneration Res; Neural Regeneration Research; 10; 4; 4-2015; 540-541
1673-5374
CONICET Digital
CONICET
url http://hdl.handle.net/11336/102697
identifier_str_mv Caltana, Laura Romina; Nieto, Maria Luisa; Brusco, Herminia Alicia; Oleanolic acid: a promising neuroprotective agent for cerebral ischemia; Shenyang Editorial Dept Neural Regeneration Res; Neural Regeneration Research; 10; 4; 4-2015; 540-541
1673-5374
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.4103/1673-5374.155414
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4424737/
info:eu-repo/semantics/altIdentifier/url/http://www.nrronline.org/article.asp?issn=1673-5374;year=2015;volume=10;issue=4;spage=540;epage=541;aulast=Laura
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Shenyang Editorial Dept Neural Regeneration Res
publisher.none.fl_str_mv Shenyang Editorial Dept Neural Regeneration Res
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
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instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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