趋化因子受体样2参与缺血性脑损伤。

R. Douglas, Alice Chen, A. Íñiguez, Juan Wang, Zhen‐lin Fu, F. Powell, G. Haddad, H. Yao
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引用次数: 8

摘要

我们通过体外和体内小鼠脑卒中模型研究了CCRL2在缺血性脑损伤中的作用。在缺血条件下,CCRL2的表达在RNA和蛋白水平上均增强。与野生型(WT)小鼠相比,CCRL2敲除(KO)小鼠的脑切片中缺血诱导的细胞死亡减少。与短暂性大脑中动脉闭塞的WT小鼠相比,CCRL2 KO小鼠的梗死体积更小,神经功能缺损减轻。我们的数据表明CCRL2参与了小鼠缺血诱导的脑损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chemokine receptor-like 2 is involved in ischemic brain injury.
We examined the role of CCRL2 in ischemic brain injury using both in vitro and in vivo mouse stroke models. The expression of CCRL2 was enhanced at both the RNA and protein levels in cultured brain slices under ischemic conditions. Ischemia-induced cell death was reduced in brain slices derived from CCRL2 knockout (KO) mice in comparison with those from wild type (WT) mice. The infarct volume was smaller and neurological deficits were attenuated in CCRL2 KO mice when compared to WT mice subjected to a transient middle cerebral artery occlusion. Our data suggest that CCRL2 is involved in ischemia-induced brain injury in mice.
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