Alterations in inflammatory mediators, oxidative stress parameters and energetic metabolism in the brain of sepsis survivor rats.
Sepsis is characterized by biochemical alterations in the central nervous system at early times and cognitive impairment at late times after induction in sepsis animal model. In order to understand at least in part the mechanism of disease, we have evaluated the effects of sepsis on cytokine levels in the cerebrospinal fluid (CSF); oxidative parameters; the activity of the electron transport chain enzymes; and creatine kinase (CK) activity in the brain of sepsis survivor rats 10 days after cecal ligation and perforation (CLP). Male Wistar rats underwent CLP with "basic support" or sham-operated. Ten days after surgery, the animals were killed and prefrontal cortex, cortex, hippocampus, striatum, cerebellum, and CSF were obtained. It was found a decrease in the levels of TNF-α (P = 0.001), IL-1β (P = 0.008), IL-6 (P = 0.038), and IL-10 (P = 0.022) in the CSF; an increase in the TBARS only hippocampus (0.027); an up-regulation in the activity of complex II (P = 0.024), III (P = 0.018), and IV (P = 0.047) only in the prefrontal cortex; a decrease in the CK activity in the cerebellum (P = 0.001) and striatum (P = 0.0001), and an increase in the hippocampus (P = 0.0001) and cortex (P = 0.0001). Oxidative stress and mitochondrial alterations observed during early times in sepsis, persisted up to 10 days after surgery. The cytokines levels during the early times were found at high levels, decreasing to low levels after 10 days. In conclusion, these findings may contribute for a better comprehension of the cognitive damage in sepsis survivor rats.
National Institute for Translational Medicine, University of Southern Santa Catarina, Criciúma, SC, Brazil.
Clarissa M
CM
Comim
Omar J
OJ
Cassol
Larissa S
LS
Constantino
Francine
F
Felisberto
Fabricia
F
Petronilho
Gislaine T
GT
Rezin
Giselli
G
Scaini
Juliana F
JF
Daufenbach
Emilio L
EL
Streck
João
J
Quevedo
Felipe
F
Dal-Pizzol
D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D003402:Creatine Kinase / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D045222:Electron Transport Chain Complex Proteins / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000378:metabolism* / Q000503:physiopathology*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D016207:Cytokines; D045222:Electron Transport Chain Complex Proteins; D018836:Inflammation Mediators; D017392:Thiobarbituric Acid Reactive Substances; D003402:Creatine Kinase