Ischemic preconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PERK pathway.

Abstract:

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.

authors

Hu YQ,Chen W,Yan MH,Lai JJ,Tang N,Wu L

doi

10.26355/eurrev_201712_14020

subject

Has Abstract

pub_date

2017-12-01 00:00:00

pages

5736-5744

issue

24

eissn

1128-3602

issn

2284-0729

journal_volume

21

pub_type

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