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A Cannabinoid CB2 Receptor Agonist Attenuated Adhesion Molecules Expression In a Mouse Ischemic/Reperfusion Injury Model
Author(s) -
Zhang Ming,
Martin Billy R,
Adler Martin W,
Razdan Raj K,
Ganea Doina,
Tuma Ronald
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.731.11
Subject(s) - agonist , extravasation , ischemia , cell adhesion molecule , pharmacology , reperfusion injury , cannabinoid receptor type 2 , cannabinoid , medicine , receptor , immunostaining , inflammation , icam 1 , anesthesia , chemistry , immunology , cannabinoid receptor , immunohistochemistry
It has been shown that leukocyte extravasation, which is mediated by adhesion molecules on both endothelial cells and leukocytes, plays an essential role in cerebral ischemic/reperfusion injury (I/R injury). The CB 2 receptor is primarily expressed by cells of immune system and its activation has been shown to attenuate cerebral I/R injury and decrease leukocyte/endothelial interactions in our lab. The purpose of this study was to determine if the protection through CB 2 receptor in cerebral I/R injury is associated with changes in adhesion molecules expression. Transient middle cerebral artery occlusion was performed in male C56BL/6 mice using an intraluminal filament method. Mice were treated with a CB 2 agonist (0–1966) at 1mg/kg i.v. or equal volume of vehicle at 1 hour before, 1 hour after or 3 hours after ischemia. Cerebral infarct volume was measured by triphenyltetrazolium chloride staining while adhesion molecules ICAM‐1 and Mac‐1 expressions were tested by immunostaining at 24 hours after ischemia. The results demonstrate that CB 2 agonist administration reduced infarct volume at all the treatment points and was associated with decreased ICAM‐1 and Mac‐1 expression in ischemic brain region.