PMID- 20940001
OWN - NLM
STAT- MEDLINE
DCOM- 20110415
LR  - 20210309
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1367
DP  - 2011 Jan 7
TI  - Ischemic postconditioning protects brain from ischemia/reperfusion injury by 
      attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt 
      pathway.
PG  - 85-93
LID - 10.1016/j.brainres.2010.10.017 [doi]
AB  - Endoplasmic reticulum (ER) stress has been implicated in the pathology of 
      cerebral ischemia. During prolonged period of stress or when the adaptive 
      response fails, apoptotic cell death ensues. Cerebral ischemic postconditioning 
      (Postcond) has been shown to reduce cerebral ischemia/reperfusion (I/R) injury in 
      both focal and global cerebral ischemia model. However, the mechanism remains to 
      be understood. This study aimed to elucidate whether Postcond attenuates brain 
      I/R damage by suppressing ER stress-induced apoptosis and if the 
      phosphatidylinositol-3kinase/Akt (PI3K/Akt) pathway is involved. A focal cerebral 
      ischemia rat model was used in the study. Rat brain infarct size and terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) positive 
      cells in ischemic penumbra were assessed after reperfusion of the brain. The 
      expressions of C/EBP-homologous protein (CHOP), caspase-12, glucose-regulated 
      protein 78 (GRP78) and the phosphorylation of Akt (Ser473) in ischemic penumbra 
      were measured after reperfusion. Our results showed that Postcond significantly 
      attenuated brain I/R injury, as shown by reduction in infarct size, cell 
      apoptosis, CHOP expression, caspase-12 activation and increase in GRP78 
      expression. LY294002, a phosphoinositide 3-kinase inhibitor, increased the number 
      of TUNEL-positive cells suppressed by Postcond in penumbra. In addition, LY294002 
      diminished the effect of Postcond on the activation of CHOP, caspase-12 and 
      GRP78. These results suggest that Postcond protects brain from I/R injury by 
      suppressing ER stress-induced apoptosis and PI3K/Akt pathway is involved.
CI  - Copyright (c) 2010 Elsevier B.V. All rights reserved.
FAU - Yuan, Yajing
AU  - Yuan Y
AD  - Department of Anesthesiology, Xiangya Hospital of Central South University, Hunan 
      410008, China.
FAU - Guo, Qulian
AU  - Guo Q
FAU - Ye, Zhi
AU  - Ye Z
FAU - Pingping, Xia
AU  - Pingping X
FAU - Wang, Na
AU  - Wang N
FAU - Song, Zongbin
AU  - Song Z
LA  - eng
PT  - Journal Article
DEP - 20101101
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Chromones)
RN  - 0 (Ddit3 protein, rat)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (GRP78 protein, rat)
RN  - 0 (Heat-Shock Proteins)
RN  - 0 (Morpholines)
RN  - 147336-12-7 (Transcription Factor CHOP)
RN  - 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 3.4.22.- (Caspase 12)
SB  - IM
MH  - Animals
MH  - Apoptosis/*physiology
MH  - Brain/*blood supply
MH  - Brain Infarction/prevention & control
MH  - Caspase 12/metabolism
MH  - Chromones/therapeutic use
MH  - Disease Models, Animal
MH  - Endoplasmic Reticulum/metabolism/*pathology
MH  - Enzyme Inhibitors/therapeutic use
MH  - Heat-Shock Proteins/metabolism
MH  - In Situ Nick-End Labeling/methods
MH  - Ischemic Postconditioning/*methods
MH  - Male
MH  - Morpholines/therapeutic use
MH  - Phosphatidylinositol 3-Kinases/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/*therapy
MH  - Signal Transduction/drug effects/*physiology
MH  - Time Factors
MH  - Transcription Factor CHOP/metabolism
EDAT- 2010/10/14 06:00
MHDA- 2011/04/19 06:00
CRDT- 2010/10/14 06:00
PHST- 2010/07/11 00:00 [received]
PHST- 2010/10/03 00:00 [revised]
PHST- 2010/10/05 00:00 [accepted]
PHST- 2010/10/14 06:00 [entrez]
PHST- 2010/10/14 06:00 [pubmed]
PHST- 2011/04/19 06:00 [medline]
AID - S0006-8993(10)02224-9 [pii]
AID - 10.1016/j.brainres.2010.10.017 [doi]
PST - ppublish
SO  - Brain Res. 2011 Jan 7;1367:85-93. doi: 10.1016/j.brainres.2010.10.017. Epub 2010 
      Nov 1.