Conflict of Interest: None of the authors or funding sources has conflict of interest.
Increased on oxidative brain injury in the diabetic rats following sepsis
Article first published online: 17 JUN 2014
Copyright © 2014 Wiley Periodicals, Inc.
Volume 68, Issue 9, pages 410–418, September 2014
How to Cite
Vieira, A., Michels, M., Florentino, D., Lauriano, A. A., Danielski, L. G., Fortunato, J. J., Barichello, T., Felipe, D.-P., Quevedo, J. and Petronilho, F. (2014), Increased on oxidative brain injury in the diabetic rats following sepsis. Synapse, 68: 410–418. doi: 10.1002/syn.21753
- Issue published online: 11 JUL 2014
- Article first published online: 17 JUN 2014
- Accepted manuscript online: 4 JUN 2014 01:38AM EST
- Manuscript Accepted: 27 MAY 2014
- Manuscript Received: 13 FEB 2014
- oxidative stress;
- brain injury;
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.