Navegando por Palavras-chave "NAD(P)H Oxidase"

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    Avaliação da produção de espécies reativas de oxigênio em ilhotas pancreáticas de camundongos knockout para o receptor Toll-4 (TLR4)
    (Universidade Federal de São Paulo (UNIFESP), 2019-05-30) Pereira, Ana Cristina Vieira [UNIFESP]; Hirata, Aparecida Emiko [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Toll-like receptors (TLRs)-like part of the innate immune system and seem to be involved in the modulation of several metabolic chronic diseases such as obesity and type 2 diabetes (DM2). Is sábido to chronic Hyperglycemia is associated with increased generation of EROs in the pancreatic islets, and this interferes with the insulin secretory process. Studies show that the delection of TLR4 receptors improves insulin resistance and chronic diseases such as obesity and type 2 diabetes (DM2). Thus, the aim of this study is to evaluate the regulation of ROS generation, in isolated pancreatic islets from KNOCKOUT mice for the receptor TLR4 (TLR4-/-), in different concentrations of glucose and/or mix of cytokines. TLR4-/- mice showed significant decrease in blood glucose levels while showed increased insulinemia compared to controls. We also observed significant increase in the relative weight of the skeletal muscle. The superoxide generation, evaluated by flow cytometry, was significantly lower compared to the control group. There were no changes in the mitochondrial superoxide and hydrogen peroxide generation. ROS geneartion stimulated by cytokines was not observed in TLR4-/- animals. The protein expression of JNK and IKKB, evaluated by Western blotting, was significantly lower in skeletal muscle of TLR4-/- animals compared to controls. However, we observed a significant increase in the protein expression of NRF2 in skeletal muscle of TLR4-/- animals comparte to controls. These results demonstrate that TLR4 participates in the redox state of the pancreatic islets, which could at least partly influence the secretory process of insulin. This mechanism appears to be mediated via JNK/IKKB and NRF2.