Cho Lab
News & Impact

You are here

Targeting CD36-mediated inflammation reduces acute brain injury in transient, but not permanent, ischemic stroke.

Journal Article
Kim EH, Tolhurst AT, Szeto HH, Cho SH.
Year Published: 
CNS Neurosci Ther. 2015 Apr;21(4):385-91. doi: 10.1111/cns.12326. Epub 2014 Sep 12.
Abstract on PubMed



The pathology of stroke consists of multiple pro-death processes, and CD36 has been suggested as a multimodal target to reduce oxidative stress and inflammation in ischemic stroke. Using CD36-deficient mice and SS-31, a cell permeable tetrapeptide known to down-regulate CD36 pathways, the current study investigated whether targeting CD36 is effective in transient and permanent ischemic stroke.


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.


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.


The study revealed that targeting CD36 has a beneficial effect on transient but not permanent focal ischemic stroke. The study thus precludes a generalized strategy targeting CD36 in ischemic stroke and suggests careful consideration of types of stroke and associated pathology in developing stroke therapies.


Conditions & Recovery

Stroke icon
Stroke is the leading cause of disability in the U.S.