Increased on oxidative brain injury in the diabetic rats following sepsis

Authors

  • Andriele Vieira,

    1. Clinical and Experimental Pathophysiology Laboratory - FICEXP, Graduate Program in Health Sciences, Universidade do Sul de Santa Catarina (UNISUL), Tubarão, Santa Catarina, Brazil
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  • Monique Michels,

    1. Clinical and Experimental Pathophysiology Laboratory - FICEXP, Graduate Program in Health Sciences, Universidade do Sul de Santa Catarina (UNISUL), Tubarão, Santa Catarina, Brazil
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  • Drielly Florentino,

    1. Clinical and Experimental Pathophysiology Laboratory - FICEXP, Graduate Program in Health Sciences, Universidade do Sul de Santa Catarina (UNISUL), Tubarão, Santa Catarina, Brazil
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  • André Antunes Lauriano,

    1. Clinical and Experimental Pathophysiology Laboratory - FICEXP, Graduate Program in Health Sciences, Universidade do Sul de Santa Catarina (UNISUL), Tubarão, Santa Catarina, Brazil
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  • Lucineia Gainski Danielski,

    1. Clinical and Experimental Pathophysiology Laboratory - FICEXP, Graduate Program in Health Sciences, Universidade do Sul de Santa Catarina (UNISUL), Tubarão, Santa Catarina, Brazil
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  • Jucelia Jeremias Fortunato,

    1. Clinical and Experimental Pathophysiology Laboratory - FICEXP, Graduate Program in Health Sciences, Universidade do Sul de Santa Catarina (UNISUL), Tubarão, Santa Catarina, Brazil
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  • Tatiana Barichello,

    1. Laboratory of Experimental Microbiology, Graduate Program in Health Sciences, Universidade do Extremo Sul Catarinense (UNESC), Criciúma, Santa Catarina, Brazil
    2. Department of Psychiatry and Behavioral Sciences, Center for Experimental Models in Psychiatry, The University of Texas Medical School at Houston, Texas
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  • Felipe Dal-Pizzol,

    1. Experimental Pathophysiology Laboratory - FISIOPAT, Graduate Program in Health Sciences, Universidade do Extremo Sul de Santa Catarina (UNESC), Criciuma, Santa Catarina, Brazil
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  • Joao Quevedo,

    1. Department of Psychiatry and Behavioral Sciences, Center for Experimental Models in Psychiatry, The University of Texas Medical School at Houston, Texas
    2. Laboratory of Neurociences, Graduate Program in Health Sciences, Universidade do Extremo Sul de Santa Catarina (UNESC), Criciuma, Santa Catarina, Brazil
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  • Fabricia Petronilho

    Corresponding author
    1. Clinical and Experimental Pathophysiology Laboratory - FICEXP, Graduate Program in Health Sciences, Universidade do Sul de Santa Catarina (UNISUL), Tubarão, Santa Catarina, Brazil
    2. Department of Psychiatry and Behavioral Sciences, Center for Experimental Models in Psychiatry, The University of Texas Medical School at Houston, Texas
    • Correspondence to: Fabricia Petronilho, Laboratório de Fisiopatologia Clinica e Experimental, Programa de Pós-Graduação em Ciências da Saúde, Universidade do Sul de Santa Catarina, 88704-900, Tubarão, SC, Brazil. E-mail: fabricia.petronilho@unisul.br

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  • Conflict of Interest: None of the authors or funding sources has conflict of interest.

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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