Acute white matter injury after experimental subarachnoid hemorrhage: potential role of lipocalin 2.
Acute white matter injury after experimental subarachnoid hemorrhage: potential role of lipocalin 2.
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DOI：
10.1161/strokeaha.114.005307
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发表时间：
2014-07
期刊：
影响因子：
8.3
通讯作者：
Xi G
中科院分区：
文献类型：
--
作者：
Egashira Y;Hua Y;Keep RF;Xi G
白色物质损伤发生在蛛网膜下腔出血（SAH）后，尚未得到很好的研究。在这项研究中，我们研究了急性白色物质损伤的小鼠SAH模型和脂质运载蛋白2（LCN 2）在这种损伤中的作用。在野生型（WT）或LCN 2敲除（LCN 2 −/−）小鼠中，通过血管内穿孔诱导SAH。Sham WT小鼠经历相同的程序而没有穿孔。SAH后24小时行MRI检查，测量白色物质中T2高信号的体积。免疫组化检测脑白色损伤。WT和LCN 2 −/−动物之间的死亡率和SAH严重程度没有显著差异。在SAH后24小时，在所有WT动物中观察到白色物质中的T2高信号（6.1±2.7与假手术中的0.06±0.07 mm 3; P<0.001），并且T2高信号的体积倾向于与SAH严重程度相关（r=0.30; P=0.055）。在患有SAH的WT动物中，在白色物质中观察到大量LCN 2阳性细胞。相比之下，LCN 2 −/−动物在SAH后几乎没有出现白色T2高信号（0.5±0.5 mm 3; P<0.001，vs. WT）。与LCN 2 −/−动物相比，WT组SAH后白色物质中轴突损伤和髓鞘降解的标记物增加（P<0.05）。蛛网膜下腔出血（SAH）24 h可引起小鼠急性白色损伤，LCN 2在SAH诱导的白色损伤中起重要作用。
White matter injury occurs after subarachnoid hemorrhage (SAH) and has not been well studied. In this study, we investigated acute white matter injury in a mouse SAH model and the role of lipocalin 2 (LCN2) in that injury. SAH was induced by endovascular perforation in wild-type (WT) or LCN2 knockout (LCN2−/−) mice. Sham WT mice underwent the same procedure without perforation. MRI was performed 24 hours after SAH and the volumes of the T2-hyperintensity in white matter were measured. Immunohistochemistry was performed to determine white matter injury. Mortality rates and SAH severity were not significantly different between WT and LCN2−/− animals. T2-hyperintensity in the white matter was observed in all WT animals at 24 hours after SAH (6.1±2.7 vs. 0.06±0.07 mm3 in sham; P<0.001), and the volume of T2-hyperintensity tended to correlate with SAH severity (r=0.30; P=0.055). In WT animals with SAH, numerous LCN2 positive cells were observed in white matter. In contrast, LCN2−/− animals scarcely developed white matter T2-hyperintensity after SAH (0.5±0.5 mm3; P<0.001, vs. WT). Markers of axonal damage and myelin degradation were increased in white matter after SAH in WT compared to those in LCN2−/− animals (P<0.05). SAH results in an acute white matter injury at 24 hours in mice, and LCN2 plays an important role in SAH-induced white matter injury.