Blocking Beta2-adrenergic Receptor Reduced Ischemia-induced Blood Brain Barrier Bamage by Regulating Hypoxia-inducible factor-1 alpha Expression during Acute Cerebral Ischemia

Sun Yanyun; Zhang Xinyu; Shen Xianzhi; Jin Xinchun

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Blocking Beta2-adrenergic Receptor Reduced Ischemia-induced Blood Brain Barrier Bamage by Regulating Hypoxia-inducible factor-1 alpha Expression during Acute Cerebral Ischemia

Sun Yanyun #,Zhang Xinyu,Shen Xianzhi,Jin Xinchun *

Institute of Neuroscience, Soochow University, 215123

*Correspondence author

#Submitted by

Subject:

Funding: Doctoral New Teacher researching Fundation of the department of education（No.No. K521507713）

Opened online: 7 December 2016

Accepted by: none

Citation: Sun Yanyun,Zhang Xinyu,Shen Xianzhi.Blocking Beta2-adrenergic Receptor Reduced Ischemia-induced Blood Brain Barrier Bamage by Regulating Hypoxia-inducible factor-1 alpha Expression during Acute Cerebral Ischemia[OL]. [ 7 December 2016] http://en.paper.edu.cn/en_releasepaper/content/4712245

Disruption of the blood brain barrier (BBB) within the thrombolytic time window is an antecedent event to intracerebral hemorrhage in ischemic stroke. Since hypoxia-inducible factor-1 alpha (HIF-1α) was discovered as a mater regulator in hypoxia, we sought to investigate the roles of HIF-1α in BBB damage as well as factors regulating HIF-1α expression after acute ischemia stroke. Our previous research results have showed that pretreatment with HIF-1α inhibitor YC-1 significantly inhibited 2-h MCAO-induced BBB damage by inhibition of occludin degradation and vascular endothelial growth factor (VEGF) mRNA upregulation. Interestingly, blocking beta2-adrenergic receptor (β2-AR) reduced ischemia-induced BBB damage by regulating HIF-1α expression in this research. More important, blocking β2-AR inhibited 2-h OGD-induced HIF-1α upregualtion and reduced occludin degradation induced by OGD-neuron media. Taken together, acute cerebral ischemia disrupts BBB by upregulating HIF-1α and activating the neurons to secret VEGF and MMP-2, while blocking β2-AR inhibited such change. These findings may provide new ideas and strategies to extend the time window of thrombolysis and reduce cerebral hemorrhage.

Keywords:cerebral ischemia; HIF-1α; β2-AR; blood brain barrier; tight junction proteins

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