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Potencial efecto neuroprotector de los agonistas LXR en la activación de autofagia de células gliales y neuronales sometidas a privación de glucosa y oxígeno

dc.rights.licenseAtribución-NoComercial-SinDerivadas 4.0 Internacional
dc.contributor.advisorArboleda Bustos, Gonzalo Humberto
dc.contributor.authorVargas Moreno, Monica Alexandra
dc.date.accessioned2023-07-27T21:32:25Z
dc.date.available2023-07-27T21:32:25Z
dc.date.issued2023-07-26
dc.identifier.urihttps://repositorio.unal.edu.co/handle/unal/84339
dc.descriptionilustraciones, diagramas, fotografías
dc.description.abstractLa enfermedad cerebrovascular es una de las causas más relevantes de morbimortalidad en el mundo. Por ello es de gran importancia el entendimiento de los mecanismos fisiopatológicos de esta enfermedad, que permitan encontrar blancos terapéuticos para mejorar la sobrevida neuronal que prosigue a la lesión isquémica. Clásicamente se hablaba de 2 tipos de muerte celular relacionadas con este tipo de lesión: necrosis y apoptosis; sin embargo, recientemente se ha encontrado una gran variedad morfológica de tipos adicionales de muerte celular, entre estas, la asociada a autofagia ha tomado gran importancia en la última década. Existe evidencia reciente del efecto neuroprotector de los agonistas de receptores X del hígado (LXR: por sus siglas en inglés, Liver X receptors) en escenarios de isquemia cerebral y de su capacidad de modular la activación de la autofagia. Se ha descrito también el papel que cumplen las células gliales en el daño neuronal que prosigue a la lesión isquémica. Debido a esto, se planteó como objetivo general analizar el efecto de agonistas LXR en la activación de procesos de autofagia en células gliales y neuronales expuestas a privación de glucosa y oxígeno como un posible blanco terapéutico para modular la respuesta celular deletérea post isquemia. Se desarrolló un modelo in vitro de isquemia celular con líneas celulares y cultivo primario de neuronas y células gliales de corteza de ratón expuestas a privación de glucosa y oxígeno pretratadas con un extracto de plantas colombianas con actividad agonista LXR, Zanthoxylum caribaeum. Encontrando que el pretratamiento con las fracciones en estudio ofrece protección ante la privación combinada de glucosa y oxígeno en líneas celulares y células gliales de cultivo primario y en estas últimas podría activar vías de autofagia evidenciado en el aumentó de los niveles de LC3II. (Texto tomado de la fuente)
dc.description.abstractCerebrovascular disease is one of the most relevant causes of morbimortality in the world. Therefore, the understanding of the physio pathological disease mechanisms that will allow the acquisition of therapeutic targets to improve neuronal survival after an ischemic lesion is of the utmost importance. Traditionally, two types of cell death were associated with this kind of lesion: necrosis and apoptosis, however as of late a great variety of morphological types of cellular death has been found, among those, the one associated with autophagy has gained great importance in the last decade. There is recent evidence of the neuroprotective effect of the Liver X receptor (LXR) agonists in scenarios of cerebral ischemia and their ability to modulate autophagy activation. The role of glial cells in neuronal damage after an ischemic injury has also been described. Due to this, the analyzing the effect of the LXR agonists on the activation of the autophagy processes on glial and neuronal cells exposed to glucose and oxygen deprivation as a possible therapeutic target to modulate the deleterious post ischemic cell response was proposed as a primary objective. An in vitro model of cellular ischemia was developed, using cell lines, neuron primary cultures, as well as glial cortex cells obtained from mice, all of which were exposed to glucose and oxygen deprivation and pretreated with and extract obtained from Colombian plants with an LXR agonist activity, Zanthoxylum caribaeum. We found that pretreatment with the studied fractions confers protection against the combined deprivation of glucose and oxygen in cell lines and in primary culture glial cells, and in the latter, might activate autophagy pathways, as demonstrated by an increase in LC3II levels.
dc.format.extent94 páginas
dc.format.mimetypeapplication/pdf
dc.language.isospa
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.ddc610 - Medicina y salud::615 - Farmacología y terapéutica
dc.subject.ddc610 - Medicina y salud::616 - Enfermedades
dc.titlePotencial efecto neuroprotector de los agonistas LXR en la activación de autofagia de células gliales y neuronales sometidas a privación de glucosa y oxígeno
dc.typeTrabajo de grado - Maestría
dc.type.driverinfo:eu-repo/semantics/masterThesis
dc.type.versioninfo:eu-repo/semantics/acceptedVersion
dc.publisher.programBogotá - Medicina - Maestría en Neurociencias
dc.contributor.researchgroupGrupo de Neurociencias-Universidad Nacional de Colombia
dc.description.degreelevelMaestría
dc.description.degreenameMagíster en Neurociencias
dc.description.researchareaMuerte celular
dc.identifier.instnameUniversidad Nacional de Colombia
dc.identifier.reponameRepositorio Institucional Universidad Nacional de Colombia
dc.identifier.repourlhttps://repositorio.unal.edu.co/
dc.publisher.facultyFacultad de Medicina
dc.publisher.placeBogotá,Colombia
dc.publisher.branchUniversidad Nacional de Colombia - Sede Bogotá
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dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.subject.decsAutofagia
dc.subject.decsAutophagy
dc.subject.decsGlioma
dc.subject.proposalAutofagia
dc.subject.proposalLXR
dc.subject.proposalIsquemia cerebral
dc.subject.proposalLC3-II
dc.subject.proposalNeuroprotección
dc.subject.proposalAutophagy
dc.subject.proposalBrain ischemia
dc.subject.proposalNeuroprotection
dc.title.translatedPotential neuroprotective effect of LXR agonists on autophagy activation on glial and neuronal cells subjected to glucose and oxygen deprivation
dc.type.coarhttp://purl.org/coar/resource_type/c_bdcc
dc.type.coarversionhttp://purl.org/coar/version/c_ab4af688f83e57aa
dc.type.contentText
dc.type.redcolhttp://purl.org/redcol/resource_type/TM
oaire.accessrightshttp://purl.org/coar/access_right/c_abf2
oaire.awardtitle“Búsqueda racional de alcaloides isoquinolínicos del género Zanthoxylum (Rutaceae) como posibles agentes neuroprotectores para el tratamiento de la enfermedad de Alzheimer"
oaire.fundernameFinanciado por MINCIENCIAS Código 110177758004, convocatoria 777-2017; RC-854 de 2017
dcterms.audience.professionaldevelopmentEstudiantes
dcterms.audience.professionaldevelopmentInvestigadores
dcterms.audience.professionaldevelopmentMaestros
dcterms.audience.professionaldevelopmentPúblico general


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