title: Correlation of acute phase inflammatory and oxidative markers with long-term cognitive impairment in sepsis survivors rats.
abstract: Oxidative damage and inflammation occur early in the brain after sepsis and are resolved when long-term cognitive impairment occurs. There is no information of a direct relation between acute levels of brain inflammation and oxidative damage and long-term cognitive deficits. We hypothesized that higher levels of early oxidative damage and inflammation are followed by long-term cognitive deficits, and this is related to a decrease in the levels of brain-derived neurotropic factor (BDNF). Wistar rats were subjected to sham operation or cecal ligation and perforation and the cerebrospinal fluid (CSF) was obtained 6 and 24 h after the determination of thiobarbituric acid-reactive species, interleukin 1 (IL-1), IL-10, and tumor necrosis factor α (TNF-α). Animals were followed until 30 days after surgery and were subjected to the step-down inhibitory avoidance (IA) task, and the hippocampus levels of BDNF were determined. At 6 h, higher CSF levels of thiobarbituric acid-reactive species and TNF-α were observed in septic animals that had a better performance in the IA task and presented higher BDNF levels in the hippocampus. At 24 h, higher CSF levels of IL-1β and TNF-α were observed in septic animals that had a worse performance in the IA task, and this was associated with lower BDNF levels. The persistence of brain inflammation during the acute phase of sepsis is associated with long-term hippocampus levels of BDNF and memory impairment in sepsis survivors.
authors.affiliation: Laboratório de Fisiopatologia Experimental and Instituto Nacional de Ciência e Tecnologia Translacional em Medicina, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, Brazil.
authors.forename: Daiane
authors.initials: D
authors.lastname: Biff
authors.forename: Fabrícia
authors.initials: F
authors.lastname: Petronilho
authors.forename: Larissa
authors.initials: L
authors.lastname: Constantino
authors.forename: Francieli
authors.initials: F
authors.lastname: Vuolo
authors.forename: Grettel J
authors.initials: GJ
authors.lastname: Zamora-Berridi
authors.forename: Dhébora Mozena
authors.initials: DM
authors.lastname: Dall'Igna
authors.forename: Clarissa M
authors.initials: CM
authors.lastname: Comim
authors.forename: João
authors.initials: J
authors.lastname: Quevedo
authors.forename: Flávio
authors.initials: F
authors.lastname: Kapczinski
authors.forename: Felipe
authors.initials: F
authors.lastname: Dal-Pizzol
mesh_terms: D000818:Animals; D003072:Cognition Disorders / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D007375:Interleukin-1 / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000378:metabolism* / Q000503:physiopathology*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D007375:Interleukin-1; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10