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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/102697
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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 |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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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