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Adropin preserves the blood-brain barrier through a Notch1/Hes1 pathway after intracerebral hemorrhage in mice.

Authors
  • Yu, Lingyan1, 2
  • Lu, Zhengyang2, 3
  • Burchell, Sherrefa2
  • Nowrangi, Derek2
  • Manaenko, Anatol2
  • Li, Xue1, 2
  • Xu, Yang2
  • Xu, Ningbo2
  • Tang, Jiping2
  • Dai, Haibin1
  • Zhang, John H2
  • 1 Department of Pharmacy, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. , (China)
  • 2 Departments of Anesthesiology and Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, California, USA.
  • 3 Departments of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital, Soochow University, Suzhou, China. , (China)
Type
Published Article
Journal
Journal of Neurochemistry
Publisher
Wiley (Blackwell Publishing)
Publication Date
Dec 01, 2017
Volume
143
Issue
6
Pages
750–760
Identifiers
DOI: 10.1111/jnc.14238
PMID: 29030969
Source
Medline
Keywords
License
Unknown

Abstract

Adropin is expressed in the CNS and plays a crucial role in the development of stroke. However, little is currently known about the effects of adropin on the blood-brain barrier (BBB) function after intracerebral hemorrhage (ICH). In this study, the role of adropin in collagenase-induced ICH was investigated in mice. At 1-h post-ICH, mice were administered with recombinant human adropin by intranasal. Brain water +content, BBB permeability, and neurological function were measured at different time intervals. Proteins were quantified using western blot analysis, and the localizations of adropin and Notch1 were visualized via immunofluorescence staining. It is shown that adropin reduced brain water content and improved neurological functions. Adropin preserved the functionality of BBB by increasing N-cadherin expression and reducing extravasation of albumin. Moreover, in vivo knockdown of Notch1 and Hes1 both abolished the protective effects of adropin. Taken together, our data demonstrate that adropin constitutes a potential treatment value for ICH by preserving BBB and improving functional outcomes through the Notch1 signaling pathway.

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