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

Targeting CD36-mediated inflammation reduces acute brain injury in transient, but not permanent, ischemic stroke.
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DOI:
10.1111/cns.12326
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发表时间:
2015-04
影响因子:
5.5
通讯作者:
Cho SH
Cho SH
中科院分区:
医学1区
文献类型:
--
作者:
Kim EH;Tolhurst AT;Szeto HH;Cho SH

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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. WT 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 post-ischemic 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.
DOI: 10.1074/jbc.m609388200
发表时间: 2007-02-16
影响因子: 4.8
作者:
Cho, Sunghee;Szeto, Hazel H.;Pinto, John T.
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