PMID- 28238791
OWN - NLM
STAT- MEDLINE
DCOM- 20180413
LR  - 20180413
IS  - 1872-9754 (Electronic)
IS  - 0197-0186 (Linking)
VI  - 108
DP  - 2017 Sep
TI  - Selol, an organic selenium donor, prevents lipopolysaccharide-induced oxidative 
      stress and inflammatory reaction in the rat brain.
PG  - 66-77
LID - S0197-0186(16)30331-X [pii]
LID - 10.1016/j.neuint.2017.02.014 [doi]
AB  - Neuroinflammation and oxidative stress are key intertwined pathological factors 
      in many neurological, particularly neurodegenerative diseases, such as 
      Alzheimer's and Parkinson's disorders as well as autism. The present study was 
      conducted to evaluate the protective effects of Selol, an organic selenium donor, 
      against lipopolysaccharide (LPS)-mediated inflammation in rat brain. The results 
      demonstrated that the peripheral administration of LPS in a dose of 100 mug/kg 
      b.w. evoked typical pathological reaction known as systemic inflammatory 
      response. Moreover, we observed elevated blood levels of thiobarbituric 
      acid-reactive substances (TBARS), a marker of oxidative stress, as well as 
      increased concentration of tumor necrosis factor-alpha (TNF-alpha) in LPS-treated 
      animals. Selol significantly prevented these LPS-evoked changes. Subsequently, 
      Selol protected against LPS-induced up-regulation of proinflammatory cytokines 
      (Tnfa, Ifng, Il6) in rat brain cortex. The molecular mechanisms through which 
      Selol prevented the neuroinflammation were associated with the inhibition of 
      oxidized glutathione (GSSG) accumulation and with an increase of 
      glutathione-associated enzymes: glutathione peroxidase (Se-GPx), glutathione 
      reductase (GR) as well as thioredoxin reductase (TrxR) activity and expression. 
      Finally, we observed that Selol administration effectively protected against 
      LPS-induced changes in the expression of brain-derived neurotrophic factor 
      (Bdnf). In conclusion, our studies indicated that Selol effectively protects 
      against LPS-induced neuroinflammation by inhibiting pro-inflammatory cytokine 
      release, by boosting antioxidant systems, and by augmenting BDNF level. 
      Therefore, Selol could be a multi-potent and effective drug useful in the 
      treatment and prevention of brain disorders associated with neuroinflammation.
CI  - Copyright (c) 2017 Elsevier Ltd. All rights reserved.
FAU - Dominiak, Agnieszka
AU  - Dominiak A
AD  - Department of Bioanalysis and Drug Analysis, Medical University of Warsaw, 
      Banacha 1 St., 02-097 Warsaw, Poland.
FAU - Wilkaniec, Anna
AU  - Wilkaniec A
AD  - Department of Cellular Signalling, Mossakowski Medical Research Centre Polish 
      Academy of Sciences, Pawinskiego 5 St., 02-106 Warsaw, Poland.
FAU - Jesko, Henryk
AU  - Jesko H
AD  - Department of Cellular Signalling, Mossakowski Medical Research Centre Polish 
      Academy of Sciences, Pawinskiego 5 St., 02-106 Warsaw, Poland.
FAU - Czapski, Grzegorz A
AU  - Czapski GA
AD  - Department of Cellular Signalling, Mossakowski Medical Research Centre Polish 
      Academy of Sciences, Pawinskiego 5 St., 02-106 Warsaw, Poland.
FAU - Lenkiewicz, Anna M
AU  - Lenkiewicz AM
AD  - Department of Cellular Signalling, Mossakowski Medical Research Centre Polish 
      Academy of Sciences, Pawinskiego 5 St., 02-106 Warsaw, Poland.
FAU - Kurek, Eliza
AU  - Kurek E
AD  - Faculty of Chemistry, Biological and Chemical Research Centre, University of 
      Warsaw, Zwirki i Wigury 101 St., 02-089 Warsaw, Poland.
FAU - Wroczynski, Piotr
AU  - Wroczynski P
AD  - Department of Bioanalysis and Drug Analysis, Medical University of Warsaw, 
      Banacha 1 St., 02-097 Warsaw, Poland.
FAU - Adamczyk, Agata
AU  - Adamczyk A
AD  - Department of Cellular Signalling, Mossakowski Medical Research Centre Polish 
      Academy of Sciences, Pawinskiego 5 St., 02-106 Warsaw, Poland. Electronic 
      address: agataadamczyk72@gmail.com.
LA  - eng
PT  - Journal Article
DEP - 20170224
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Selenium Compounds)
RN  - 176669-95-7 (selol)
RN  - H6241UJ22B (Selenium)
SB  - IM
MH  - Animals
MH  - Brain/drug effects/*metabolism
MH  - Female
MH  - Inflammation/drug therapy/metabolism
MH  - Inflammation Mediators/antagonists & inhibitors/*metabolism
MH  - Lipopolysaccharides/*toxicity
MH  - Oxidative Stress/drug effects/*physiology
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - Selenium/*metabolism
MH  - Selenium Compounds/*pharmacology/therapeutic use
OTO - NOTNLM
OT  - Lipopolysaccharide
OT  - Neurodegenerative disease
OT  - Neuroinflammation
OT  - Organic selenium compound
OT  - Selenoenzyme
OT  - Selol
EDAT- 2017/02/28 06:00
MHDA- 2018/04/14 06:00
CRDT- 2017/02/28 06:00
PHST- 2016/09/21 00:00 [received]
PHST- 2017/02/17 00:00 [revised]
PHST- 2017/02/22 00:00 [accepted]
PHST- 2017/02/28 06:00 [pubmed]
PHST- 2018/04/14 06:00 [medline]
PHST- 2017/02/28 06:00 [entrez]
AID - S0197-0186(16)30331-X [pii]
AID - 10.1016/j.neuint.2017.02.014 [doi]
PST - ppublish
SO  - Neurochem Int. 2017 Sep;108:66-77. doi: 10.1016/j.neuint.2017.02.014. Epub 2017 
      Feb 24.