PMID- 29272010
OWN - NLM
STAT- MEDLINE
DCOM- 20191219
LR  - 20191219
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 21
IP  - 24
DP  - 2017 Dec
TI  - Ischemic preconditioning protects brain from ischemia/reperfusion injury by 
      attenuating endoplasmic reticulum stress-induced apoptosis through PERK pathway.
PG  - 5736-5744
LID - 14020 [pii]
LID - 10.26355/eurrev_201712_14020 [doi]
AB  - OBJECTIVE: The purpose of this study was to explore the effects of cerebral 
      ischemic preconditioning which can decrease brain ischemia/reperfusion (I/R) 
      injury by inhibiting endoplasmic reticulum (ER) stress-induced apoptosis. 
      MATERIALS AND METHODS: The focal cerebral ischemia rat was selected as the 
      experimental model. Terminal deoxynucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL) positive cells in ischemic penumbra were assessed after cerebral 
      reperfusion. We assessed terminal deoxynucleotidyl transferase-mediated dUTP nick 
      end labeling (TUNEL) positive cells and measured the expressions of 
      phosphorylation PERK (p-PERK), glucose-regulated protein 78 (GRP78), activating 
      transcription factor-4 (ATF4) and caspase-12 in ischemic penumbra after cerebral 
      reperfusion. RESULTS: We showed that the infarct sizes can be reduced due to the 
      preconditioning under the influence of brain ischemia after reperfusion. The 
      effect of preconditioning on the expression of ER stress proteins suggested the 
      expressions of the 4 proteins p-PERK, ATF4, caspase-12 and GRP78 in the penumbra 
      cortex by immunohistochemistry and Western blot increased after cerebral 
      ischemia. Significant reduction of the number of TUNEL-positive cells was in the 
      penumbra cortex of the preconditioning group. CONCLUSIONS: We found that cerebral 
      ischemic preconditioning can protect the brain from I/R injury by inhibiting ER 
      stress-induced apoptosis; the pathway of PERK is involved.
FAU - Hu, Y-Q
AU  - Hu YQ
AD  - Department of Neurology, The First Affiliated Hospital of Guangxi University of 
      Chinese Medicine, Nanning, Guangxi, China. Yanwo7073@163.com.
FAU - Chen, W
AU  - Chen W
FAU - Yan, M-H
AU  - Yan MH
FAU - Lai, J-J
AU  - Lai JJ
FAU - Tang, N
AU  - Tang N
FAU - Wu, L
AU  - Wu L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - EC 2.7.11.1 (PERK kinase)
RN  - EC 2.7.11.1 (eIF-2 Kinase)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Brain/metabolism
MH  - *Brain Ischemia/metabolism
MH  - *Endoplasmic Reticulum Stress
MH  - In Situ Nick-End Labeling
MH  - Phosphorylation
MH  - Rats
MH  - *Reperfusion Injury/metabolism
MH  - *eIF-2 Kinase/metabolism
EDAT- 2017/12/23 06:00
MHDA- 2019/12/20 06:00
CRDT- 2017/12/23 06:00
PHST- 2017/12/23 06:00 [entrez]
PHST- 2017/12/23 06:00 [pubmed]
PHST- 2019/12/20 06:00 [medline]
AID - 14020 [pii]
AID - 10.26355/eurrev_201712_14020 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2017 Dec;21(24):5736-5744. doi: 
      10.26355/eurrev_201712_14020.