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Doctoral Thesis
DOI
10.11606/T.42.2018.tde-20022018-150159
Document
Author
Full name
Mariana Rodrigues Davanso Braga
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2017
Supervisor
Committee
Curi, Rui (President)
Boaventura, Maria Fernanda Cury
Gorjão, Renata
Martins, Joilson de Oliveira
Santos, Marinilce Fagundes dos
Title in Portuguese
Efeitos dos ácidos graxos na função de macrófagos de camundongos com diabetes tipo I induzido.
Keywords in Portuguese
Ácidos graxos
DHA
Diabetes mellitus tipo I
Estreptozotocina
Inflamação
Macrófago
Ômega-3
Abstract in Portuguese
O diabetes mellitus tipo I (DMI) é uma doença crônica autoimune caracterizada por hiperglicemia devido à destruição das células beta pancreáticas produtoras de insulina. Ao final de 30 dias da indução do diabetes por estreptozotocina, os macrófagos peritoneais residentes dos animais diabéticos apresentaram aumento de RNAm de citocinas e quimiocinas inflamatórias, secreção de óxido nítrico, expressão de NLRP3, iNOS e PARP1 e da atividade da via glicolítica. Perfil pró-inflamatório também foi observado em macrófagos peritoneais de animais NOD (non-obese diabetic). Camundongos diabéticos deficientes em NLRP3 (NLRP3 KO) apresentaram diminuição na expressão de iNOS, PARP1 e na produção de NO em relação aos macrófagos dos animais diabéticos selvagens. O estado diabético tipo I influenciou o perfil dos macrófagos peritoneais residentes, causando aumento na produção de NO, via NLRP3-PARP1-iNOS, expressão de citocinas pró-inflamatórias, receptores de quimiocinas e da atividade glicolítica. O tratamento com DHA (ômega-3) ex-vivo reverteu este perfil e atenuou o quadro pró-inflamatório por diminuição da produção de NO e da expressão de citocinas pró-inflamatórias.
Title in English
Effects of fatty acids in macrophage function from type I diabetic mice.
Keywords in English
DHA
Fatty acids
Inflammation
Macrophage
Omega-3
Streptozotocin
Type I diabetes mellitus
Abstract in English
Type I diabetes mellitus (DMI) is a chronic autoimmune disease characterized by hyperglycemia due to the destruction of insulin-producing pancreatic beta cells. At the end of 30 days after type I diabetes induced by streptozotocin, macrophages from diabetic animals had increased expressions of inflammatory cytokines and chemokines, secretion of nitric oxide, expression of NLRP3, iNOS and PARP1, and glycolytic activity compared to the cells from control animals. Proinflammatory features was also observed in peritoneal macrophages of NOD (non-obese diabetic) animals. Macrophages from NLRP3 deficient diabetic mice (NLRP3 KO) had decreased expression of iNOS, PARP1 and of NO production when compared to cells from wild type animals. The type I diabetic state led to a proinflammatory feature in resident peritoneal macrophages by increasing NO production, via the NLRP3-PARP1-iNOS pathway, expressions of proinflammatory cytokines, chemokine receptors and glycolytic activity. In contrast, ex-vivo treatment with DHA (omega-3) reversed this profile and attenuated the proinflammatory state by reducing NO production and expression of proinflammatory cytokines.
 
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Publishing Date
2018-02-20
 
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