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Lithium Posttreatment Alleviates Blood-Brain Barrier Injury After Intracerebral Hemorrhage in Rats.

Authors
  • Li, Weishan1
  • Li, Rui1
  • Zhao, Sha1
  • Jiang, Cheng1
  • Liu, Zhen1
  • Tang, Xiaobo2
  • 1 College of Pharmacy, Harbin Medical University, Department of Biopharmaceutical Sciences (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), PR China. , (China)
  • 2 College of Pharmacy, Harbin Medical University, Department of Biopharmaceutical Sciences (State-Province Key Laboratories of Biomedicine-Pharmaceutics of China), PR China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Neuroscience
Publication Date
May 21, 2018
Volume
383
Pages
129–137
Identifiers
DOI: 10.1016/j.neuroscience.2018.05.001
PMID: 29775701
Source
Medline
Keywords
License
Unknown

Abstract

Vasogenic cerebral edema formation after blood-brain barrier (BBB) damage aggravates the devastating consequences of intracerebral hemorrhage (ICH). The present study aims to probe into a therapeutic method on BBB preservation after ICH with a glycogen synthase kinase-3β (GSK-3β) inhibitor, lithium. Intrastriatal infusion of semicoagulated autologous whole blood or sham surgery was performed on male Sprague-Dawley (SD) rats (n = 208). Experimental animals received administration of 4,6-disubstitutedpyrrolo-pyrimidine (TWS119), lithium alone or in combination with a phosphatidylinositol 3-kinase inhibitor, wortmannin, after ICH. Behavioral tests, brain edema, and BBB permeability were determined at 24 and 72 h after surgery. Expressions of Akt, GSK-3β, β-catenin, claudin-1 and claudin-3 were evaluated via Western blots. Our results showed lithium alone posttreatment activated GSK-3β, therefore increasing active β-catenin and claudin-1 and claudin-3 expressions, which were accompanied with improved BBB integrity and ameliorated sensorimotor deficits and brain edema in ICH animals. We concluded that lithium alone reduced BBB damage after ICH, likely through regulating Akt/GSK-3β pathway and stabilizing β-catenin.

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