Increased on oxidative brain injury in the diabetic rats following sepsis |
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| Authors: | Andriele Vieira Monique Michels Drielly Florentino André Antunes Lauriano Lucineia Gainski Danielski Jucelia Jeremias Fortunato Tatiana Barichello Dal‐Pizzol Felipe Joao Quevedo Fabricia Petronilho |
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| Affiliation: | 1. Clinical and Experimental Pathophysiology Laboratory ‐ FICEXP, Graduate Program in Health Sciences, Universidade do Sul de Santa Catarina (UNISUL), , Tubar?o, Santa Catarina, Brazil;2. Laboratory of Experimental Microbiology, Graduate Program in Health Sciences, Universidade do Extremo Sul Catarinense (UNESC), , Criciúma, Santa Catarina, Brazil;3. Department of Psychiatry and Behavioral Sciences, Center for Experimental Models in Psychiatry, The University of Texas Medical School at Houston, , Texas;4. Experimental Pathophysiology Laboratory ‐ FISIOPAT, Graduate Program in Health Sciences, Universidade do Extremo Sul de Santa Catarina (UNESC), , Criciuma, Santa Catarina, Brazil;5. Laboratory of Neurociences, Graduate Program in Health Sciences, Universidade do Extremo Sul de Santa Catarina (UNESC), , Criciuma, Santa Catarina, Brazil |
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| Abstract: | Diabetes has been the subject of recent research by increase susceptibility to infections, thus the aim of this study was to evaluate in animal model of diabetes induced by alloxan (ALX) and subjected to sepsis the parameters of oxidative stress on the brain. Diabetes was induced in Wistar rats by ALX (150 mg/kg), and 15 days after, sepsis was induced by cecal ligation and puncture (CLP). The myeloperoxidase activity (MPO), nitrite/nitrate, oxidative damage parameters, and the activity of superoxide dismutase (SOD) and catalase (CAT) were measured in the cerebellum, hippocampus, striatum, prefrontal, and cortex in 6, 12, and 24 h after CLP. The results showed the potentiation of diabetes with sepsis. We verified these potentiation on MPO levels in the cerebellum, hippocampus, and prefrontal and an increase of the nitrite/nitrate concentration in the hippocampus, striatum, prefrontal, and cortex in 24 h after sepsis surgery. To oxidative damage, we verified in 6 h an increase on lipid and protein damage parameters in the striatum and hippocampus in 24 h. When we associate sepsis and diabetes, the SOD and CAT activity not were altered. Thus, diabetes associated with sepsis exacerbates brain damage resulting from inflammation and oxidative stress in brain. Synapse, 2014 . © 2014 Wiley Periodicals, Inc. |
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| Keywords: | sepsis oxidative stress brain injury diabetes inflammation |
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