凝血酶诱导的脑出血：蛋白酶激活受体-1 的作用。
Thrombin-induced cerebral hemorrhage: role of protease-activated receptor-1.
机构信息
Department of Neurosurgery, University of Michigan, 109 Zina Pitcher Place, Ann Arbor, MI, 48109-2200, USA.
出版信息
Transl Stroke Res. 2014 Aug;5(4):472-5. doi: 10.1007/s12975-013-0288-8. Epub 2013 Sep 21.
Abstract
Thrombin causes blood-brain barrier disruption, and this study examined whether thrombin can cause brain hemorrhage through protease-activated receptor-1 (PAR-1). Male wild type and PAR-1 knockout mice had an intracerebral injection of thrombin or saline. Mice then underwent serial T2 magnetic resonance imaging and were euthanized for brain hemoglobin, iron, and interleukin-1β measurements. Thrombin caused massive T2 lesions and brain hemorrhage in wild type mice. These effects were markedly reduced in PAR-1 knockout mice. Thrombin also increased brain interleukin-1β, and this was absent in PAR-1 knockout mice. In conclusion, thrombin increases interleukin-1β levels and induces intracerebral hemorrhage through PAR-1 activation.
摘要
凝血酶可导致血脑屏障破坏，本研究旨在探讨凝血酶是否可通过蛋白酶激活受体-1（PAR-1）引起脑出血。雄性野生型和 PAR-1 敲除小鼠接受脑内凝血酶或生理盐水注射。然后对小鼠进行连续 T2 磁共振成像，并进行脑血红蛋白、铁和白细胞介素-1β测量后处死。凝血酶可导致野生型小鼠出现大面积 T2 病变和脑出血，而 PAR-1 敲除小鼠的这些作用明显减弱。凝血酶还可增加脑内白细胞介素-1β，而 PAR-1 敲除小鼠中则不存在这种情况。总之，凝血酶通过 PAR-1 激活增加白细胞介素-1β水平并诱导脑出血。
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