Mice deficient in Mac-1 (CD11b/CD18) are less susceptible to cerebral ischemia/reperfusion injury
Mice deficient in Mac-1 (CD11b/CD18) are less susceptible to cerebral ischemia/reperfusion injury
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DOI：
10.1161/01.str.30.1.134
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发表时间：
1999-01-01
期刊：
影响因子：
8.3
通讯作者：
Mayadas, TN
中科院分区：
文献类型：
--
作者：
Soriano, SG;Coxon, A;Mayadas, TN
背景和目的--巨噬细胞-1抗原（Mac-l）（CD 11b/CD 18）是一种白细胞β 2整合素，可促进中性粒细胞粘附、跨内皮迁移、吞噬作用和呼吸爆发，所有这些都可能介导缺血性脑组织再灌注损伤。为探讨Mac-1在脑缺血再灌注过程中的作用，我们分析了Mac-1基因缺陷小鼠对短暂局灶性脑缺血的影响。方法将Mac-1基因缺陷小鼠（n=12）和野生型小鼠（n=11）通过阻断左侧大脑中动脉3 h，再灌注21 h，造成短暂局灶性脑缺血/再灌注模型。用激光多普勒血流计测定局部脑血流量。脑切片用2%氯化2，3，5-三苯基四唑染色以确定梗塞体积。结果-与野生型组相比，Mac-1缺陷小鼠的梗死体积减少了26%（P
Background and Purpose-Macrophage-1 antigen (Mac-l) (CD11b/CD18), a leukocyte beta 2 integrin, facilitates neutrophil adhesion, transendothelial migration, phagocytosis, and respiratory burst, all of which may mediate reperfusion-induced injury to ischemic brain tissue in conditions such as stroke. To determine the role of Mac-1 during ischemia and reperfusion in the brain, we analyzed the effect of transient focal cerebral ischemia in mice genetically engineered with a specific deficiency in Mac-1.Methods Transient focal ischemia/reperfusion was induced by occluding the left middle cerebral artery for 3 hours followed by a 21-hour reperfusion period in Mac-l-deficient (n=12) and wild-type (n=11)mice. Regional cerebral blood flow was determined with a laser-Doppler flowmeter. Brain sections were stained with 2% 2,3,5-triphenyltetrazolium chloride to determine the infarct volume. Neutrophil accumulation was determined by staining the brain sections with dichloroacetate esterase to identify neutrophils.Results-Compared with the wild-type cohort, Mac-l-deficient mice had a 26% reduction in infarction volume (P