Ischemic postconditioning enhances glycogen synthase kinase-3β expression and alleviates cerebral ischemia/reperfusion injury

Bo Zhao; Wenwei Gao; Jiabao Hou; Yang Wu; Zhongyuan Xia

doi:10.3969/j.issn.1673-5374.2012.19.010

Ischemic postconditioning enhances glycogen synthase kinase-3β expression and alleviates cerebral ischemia/reperfusion injury

Neural Regen Res. 2012 Jul 5;7(19):1507-12. doi: 10.3969/j.issn.1673-5374.2012.19.010.

Authors

Bo Zhao¹, Wenwei Gao², Jiabao Hou¹, Yang Wu¹, Zhongyuan Xia¹

Affiliations

¹ Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
² Department of Intensive Care Unit, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.

PMID: 25657687
PMCID: PMC4308783
DOI: 10.3969/j.issn.1673-5374.2012.19.010

Abstract

The present study established global brain ischemia using the four-vessel occlusion method. Following three rounds of reperfusion for 30 seconds, and occlusion for 10 seconds, followed by reperfusion for 48 hours, infarct area, the number of TUNEL-positive cells and Bcl-2 expression were significantly reduced. However, glycogen synthase kinase-3β activity, cortical Bax and caspase-3 expression significantly increased, similar to results following ischemic postconditioning. Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity, a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway, which reduces caspase-3 expression to protect the brain against ischemic injury.

Keywords: apoptosis; cerebral ischemia/reperfusion; glycogen synthase kinase-3β; ischemic postconditioning; ischemic preconditioning; neural regeneration.