PMID- 23603768
OWN - NLM
STAT- MEDLINE
DCOM- 20140116
LR  - 20130617
IS  - 1540-0514 (Electronic)
IS  - 1073-2322 (Linking)
VI  - 40
IP  - 1
DP  - 2013 Jul
TI  - Correlation of acute phase inflammatory and oxidative markers with long-term 
      cognitive impairment in sepsis survivors rats.
PG  - 45-8
LID - 10.1097/SHK.0b013e3182959cfa [doi]
AB  - 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 alpha (TNF-alpha). 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-alpha 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-1beta and TNF-alpha 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.
FAU - Biff, Daiane
AU  - Biff D
AD  - Laboratorio de Fisiopatologia Experimental and Instituto Nacional de Ciencia e 
      Tecnologia Translacional em Medicina, Programa de Pos-Graduacao em Ciencias da 
      Saude, Unidade Academica de Ciencias da Saude, Universidade do Extremo Sul 
      Catarinense, Criciuma, Brazil.
FAU - Petronilho, Fabricia
AU  - Petronilho F
FAU - Constantino, Larissa
AU  - Constantino L
FAU - Vuolo, Francieli
AU  - Vuolo F
FAU - Zamora-Berridi, Grettel J
AU  - Zamora-Berridi GJ
FAU - Dall'Igna, Dhebora Mozena
AU  - Dall'Igna DM
FAU - Comim, Clarissa M
AU  - Comim CM
FAU - Quevedo, Joao
AU  - Quevedo J
FAU - Kapczinski, Flavio
AU  - Kapczinski F
FAU - Dal-Pizzol, Felipe
AU  - Dal-Pizzol F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Interleukin-1)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
SB  - IM
MH  - Animals
MH  - Cognition Disorders/*metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Interleukin-1/metabolism
MH  - Interleukin-10/metabolism
MH  - Male
MH  - Rats
MH  - Rats, Wistar
MH  - Sepsis/*metabolism/*physiopathology
MH  - Thiobarbituric Acid Reactive Substances/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2013/04/23 06:00
MHDA- 2014/01/17 06:00
CRDT- 2013/04/23 06:00
PHST- 2013/04/23 06:00 [entrez]
PHST- 2013/04/23 06:00 [pubmed]
PHST- 2014/01/17 06:00 [medline]
AID - 10.1097/SHK.0b013e3182959cfa [doi]
PST - ppublish
SO  - Shock. 2013 Jul;40(1):45-8. doi: 10.1097/SHK.0b013e3182959cfa.