CXCR4 Antagonist AMD3100 Protects Blood―Brain Barrier Integrity and Reduces Inflammatory Response After Focal Ischemia in Mice

Inflammatory response plays a critical role in propagating tissue damage after focal cerebral ischemia. CXCL12 is a key chemokine for leukocyte recruitment. However, the role of CXCL12 and its receptor CXCR4 in ischemia-induced inflammatory response is unclear. Here we use the pharmacological antago...

Full description

Saved in:
Bibliographic Details
Published in:Stroke (1970) 2013, Vol.44 (1), p.190-197
Main Authors: JUN HUANG, YANING LI, YAOHUI TANG, GUANGHUI TANG, YANG, Guo-Yuan, YONGTING WANG
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood-Brain Barrier - drug effects
Blood-Brain Barrier - pathology
Brain Ischemia - drug therapy
Brain Ischemia - metabolism
Brain Ischemia - pathology
Heterocyclic Compounds - pharmacology
Heterocyclic Compounds - therapeutic use
Inflammation - metabolism
Inflammation - pathology
Inflammation - prevention & control
Male
Medical sciences
Mice
Neurology
Neuropharmacology
Neuroprotective agent
Neuroprotective Agents - pharmacology
Neuroprotective Agents - therapeutic use
Neutrophil Infiltration - drug effects
Neutrophil Infiltration - physiology
Pharmacology. Drug treatments
Receptors, CXCR4 - antagonists & inhibitors
Vascular diseases and vascular malformations of the nervous system
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Inflammatory response plays a critical role in propagating tissue damage after focal cerebral ischemia. CXCL12 is a key chemokine for leukocyte recruitment. However, the role of CXCL12 and its receptor CXCR4 in ischemia-induced inflammatory response is unclear. Here we use the pharmacological antagonist of CXCR4, AMD3100, to investigate the function of CXCL12/CXCR4 in regulating inflammatory response during acute ischemia. Adult male CD-1 mice (n=184) underwent permanent suture middle cerebral artery occlusion (MCAO). AMD3100 was injected for 3 days (1 mg/kg/day) after MCAO. Brain water content, infarct volume, neurological score, and myeloperoxidase (MPO) expression and activity were examined at 24, 48, and 72 hours after MCAO. Proinflammatory cytokine RNA and protein levels in brain tissue were measured by RT-PCR and enzyme linked immunosorbent assay. Neurological score was greatly improved in AMD3100-treated mice compared with the control mice 3 days after MCAO (P
ISSN:0039-2499
1524-4628
DOI:10.1161/strokeaha.112.670299