title: Increased on oxidative brain injury in the diabetic rats following sepsis.
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.
authors.affiliation: Clinical and Experimental Pathophysiology Laboratory - FICEXP, Graduate Program in Health Sciences, Universidade do Sul de Santa Catarina (UNISUL), Tubarão, Santa Catarina, Brazil.
authors.forename: Andriele
authors.initials: A
authors.lastname: Vieira
authors.forename: Monique
authors.initials: M
authors.lastname: Michels
authors.forename: Drielly
authors.initials: D
authors.lastname: Florentino
authors.forename: André Antunes
authors.initials: AA
authors.lastname: Lauriano
authors.forename: Lucineia Gainski
authors.initials: LG
authors.lastname: Danielski
authors.forename: Jucelia Jeremias
authors.initials: JJ
authors.lastname: Fortunato
authors.forename: Tatiana
authors.initials: T
authors.lastname: Barichello
authors.forename: Felipe
authors.initials: F
authors.lastname: Dal-Pizzol
authors.forename: Joao
authors.initials: J
authors.lastname: Quevedo
authors.forename: Fabricia
authors.initials: F
authors.lastname: Petronilho
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000378:metabolism*; D008297:Male; D009566:Nitrates / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D050050:Protein Carbonylation; D011897:Random Allocation; D017208:Rats, Wistar; D018805:Sepsis / Q000150:complications* / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D009566:Nitrates; D009573:Nitrites; D017392:Thiobarbituric Acid Reactive Substances; D002374:Catalase; D009195:Peroxidase; D013482:Superoxide Dismutase
keywords: brain injury; diabetes; inflammation; oxidative stress; sepsis