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Master's Dissertation
DOI
https://doi.org/10.11606/D.17.2020.tde-04102019-162304
Document
Author
Full name
Alexandre Gomes de Macedo Maganin
E-mail
Institute/School/College
Knowledge Area
Date of Defense
Published
Ribeirão Preto, 2019
Supervisor
Committee
Cunha, Thiago Mattar (President)
Elias, Lucila Leico Kagohara
Gomes, Felipe Villela
Verri Junior, Waldiceu Aparecido
Title in Portuguese
Papel da quinurenina 3-monooxigenase expressa em astrócitos da medula espinal na manutenção da dor neuropática
Keywords in Portuguese
Astrócitos
Neuropatia
Via das quinureninas
Abstract in Portuguese
A dor neuropática é causada por lesão ou doenças associadas ao sistema nervoso somatossensorial. Já é sabido que a ativação de células gliais (microglia / astrócitos / oligodendrócitos) na medula espinhal parece desempenhar um papel determinante na indução/ manutenção da dor neuropática; descobriu-se que os astrócitos sofrem alterações no seu funcionamento, após danos nos nervos periféricos, e desempenham um papel na sensibilização das vias nociceptivas, atuando na manutenção da dor neuropática. Essas alterações podem estar relacionadas com a via metabólica da quinurenina (KMP), sistema catabólico ligado ao processo fisiopatológico. As quinureninas (Kyn) neuroativas são geradas pelo catabolismo oxidativo do aminoácido triptofano nos tecidos periféricos e no sistema nervoso central (SNC). Distúrbios no metabolismo de Kyn foram relacionados em várias doenças humanas, como depressão, esquizofrenia, doença de Alzheimer e Huntington. Além disso, Kyn pode ser convertido em vários metabólitos através da quinurenina-3-monooxigenase (KMO), que possuem ação neurotóxica. Estudo anterior do nosso grupo de pesquisa identificou que, após a lesão do nervo periférico, há uma regulação positiva do KMP, levando a um aumento de Kyn no plasma, que parece estar envolvido na manutenção da dor neuropática. A KMO é a enzima "downstream" limitante da velocidade na via da quinurenina que metaboliza oxidativamente Kyn em 3-hidroxiquinurenina (3-Hk), porém os mecanismos pelos quais Kyn periférica medeia a dor neuropática ainda não foram esclarecidos. Dentro deste contexto nossa hipótese é que a manutenção da dor neuropática é dependente do aumento de KMO presente na medula espinhal, que oxida a Kyn periférica.
Title in English
Paper of quinurenine 3-monoxygenase expressed in spinal cord astrocytes in the maintenance of neuropathic pain
Keywords in English
Astrocytes
Neuropathy
Via of the quinureninas
Abstract in English
Neuropathic pain is part of the lesion or system related to the somatosensory nervous system. It is already known that the activation of glial cells (microglia / astrocytes / oligodendrocytes) in the spinal cord seems to play a decisive role in the induction / maintenance of neuropathic pain; it was discovered that the astrocytes suffered alterations in the functioning, after the injection in the peripheral nerves, and played a role in the sensitization of the nociceptive pathways, acting in the maintenance of neuropathic pain. These changes may be related to the metabolic kinurenine (KMP), a catabolic system linked to the pathophysiological process. Neuroactive kynurenins (Kyn) are generated by the oxidative catabolism of the amino acid tryptophan in the peripheral and central nervous system (CNS) systems. Nonmetabolism disorders of Kyn have been reported in several human diseases such as depression, schizophrenia, Alzheimer's disease and Huntington's. In addition, Kyn can be converted into various metabolites through kinurenine-3-monooxygenase (KMO), which has neurotoxic action. Our previous study identified a positive KMP pressure following peripheral nerve injury, leading to increased plasma Kyn, which appears to be involved in the maintenance of neuropathic pain. KMO is a "downstream" enzyme, which can be used in the oxidative metabolism of 3-hydroxyquinurenine (3-Hk), that is, the peripheral Kyn of the neuropathic has not yet been clarified. In this context, we are maintaining the neuropathic is dependent on the growth of KMO present in the spinal cord, which oxidizes to peripheral Kyn.
 
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Publishing Date
2020-04-29
 
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