• Amanda V Steckert, Clarissa M Comim, Francielle Mina, Bruna P Mendonça, Diogo Dominguini, Gabriela K Ferreira, Milena Carvalho-Silva, Júlia S Vieira, Emilio L Streck, João Quevedo, and Felipe Dal-Pizzol.
• Laboratory of Neurosciences, National Institute for Translational Medicine (INCT-TM), Center of Excellence in Applied Neurosciences of Santa Catarina (NENASC), Postgraduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, 88806-000, Criciúma, Santa Catarina, Brazil; Laboratory of Experimental Pathophysiology, National Institute for Translational Medicine (INCT-TM), Center of Excellence in Applied Neurosciences of Santa Catarina (NENASC), Postgraduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, 88806-000, Criciúma, Santa Catarina, Brazil.
• Synapse. 2013 Nov 1;67(11):786-93.

AbstractCentral nervous system (CNS) dysfunction secondary to sepsis is characterized by long-term cognitive impairment. It was observed that oxidative damage, energetic metabolism impairment, and cytokine level alteration seen in early times in an animal model of sepsis may persist for up to 10 days and might be associated with cognitive damage. In order to understand these mechanisms, at least in part, we evaluated the effects of sepsis on cytokine levels in the cerebrospinal fluid (CSF), oxidative parameters, and energetic metabolism in the brain of rats at both 30 and 60 days after sepsis induction by cecal ligation and perforation (CLP). To this aim, male Wistar rats underwent CLP with "basic support" or were sham-operated. Both 30 and 60 days after surgery, the CSF was collected and the animals were killed by decapitation. Then, the prefrontal cortex, hippocampus, striatum, and cortex were collected. Thirty days after surgery, an increase of IL-6 level in the CSF; an increase in the thiobarbituric acid-reactive species (TBARS) in prefrontal cortex and a decrease in hippocampus, striatum, and cortex; a decrease of carbonyl protein formation only in prefrontal cortex and an increase in striatum; and an increase in the complex IV activity only in hippocampus were observed. Sixty days after sepsis, an increase of TNF-α level in the CSF; a decrease of TBARS only in hippocampus; an increase of carbonyl protein formation in striatum; and a decrease of complex I activity in prefrontal cortex, hippocampus, and striatum were observed. These findings may contribute to understanding the role of late cognitive impairment. Further studies may address how these findings interact during sepsis development and contribute to CNS dysfunction.Copyright © 2013 Wiley Periodicals, Inc.

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