Open AccessTargeting CD 36‐Mediated Inflammation Reduces Acute Brain Injury in Transient, but not Permanent, Ischemic Stroke
Author(s) -
Kim EunHee,
Tolhurst Aaron T.,
Szeto Hazel H.,
Cho SungHee
Publication year - 2015
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12326
Subject(s) - cd36 , medicine , stroke (engine) , ischemia , inflammation , ccr2 , brain ischemia , cardiology , anesthesia , receptor , chemokine , chemokine receptor , mechanical engineering , engineering
Summary Aims The pathology of stroke consists of multiple pro‐death processes, and CD 36 has been suggested as a multimodal target to reduce oxidative stress and inflammation in ischemic stroke. Using CD 36‐deficient mice and SS ‐31, a cell permeable tetrapeptide known to down‐regulate CD 36 pathways, the current study investigated whether targeting CD 36 is effective in transient and permanent ischemic stroke. Methods Wild‐type or CD36‐deficient mice were subjected to either 30‐min transient or permanent focal ischemic stroke. In parallel, a cohort of mice subjected to either transient or permanent stroke received either vehicle or 5 mg/kg of SS‐31. Monocyte chemoattractant protein‐1 (MCP‐1) and its receptor CCR2, mRNA levels, and infarct volume and percent hemispheric swelling were measured in the postischemic brain. Results CD36 deficiency or SS‐31 treatment significantly attenuated MCP‐1 or CCR2 mRNA up‐regulation and injury size in the transient ischemic stroke. However, the approaches failed to show the protective effect in permanent ischemic stroke. Conclusion The study revealed that targeting CD 36 has a beneficial effect on transient but not permanent focal ischemic stroke. The study thus precludes a generalized strategy targeting CD 36 in ischemic stroke and suggests careful consideration of types of stroke and associated pathology in developing stroke therapies.