Graduate School of Humanities and Sciences, Ochanomizu University, Ohtsuka, Bunkyo-ku, Tokyo, Japan; Institute for Human Life Science, Ochanomizu University, Ohtsuka, Bunkyo-ku, Tokyo, Japan.
Institute for Human Life Science, Ochanomizu University, Ohtsuka, Bunkyo-ku, Tokyo, Japan.
Brain Res. 2023 Nov 1;1818:148511. doi: 10.1016/j.brainres.2023.148511. Epub 2023 Jul 26.
Effective blood coagulation prevents inflammation and neuronal loss after brain injury. 2-Carba-cyclic phosphatidic acid (2ccPA), a biotherapeutic for brain injury, inhibits blood extravasation resulting from blood-brain barrier breakdown. However, the hemostasis mechanism of 2ccPA remains unclear. We determined the effects of 2ccPA-injection on blood coagulation and fibrinolysis using a needle-induced brain injury model. 2ccPA suppressed the expression of platelet degranulation-related genes. Immediately after brain injury, 2ccPA increased CD41 platelet aggregation around the lesions and promoted fibrin aggregation. Additionally, 2ccPA supported fibrinolysis by upregulating plasminogen activator expression. These results suggest the acute effects of 2ccPA on brain hemostasis.
有效的血液凝固可以预防脑损伤后的炎症和神经元丢失。2-碳环磷酸酰基磷脂酸(2ccPA)是一种治疗脑损伤的生物疗法,可抑制血脑屏障破坏导致的血液外渗。然而,2ccPA 的止血机制尚不清楚。我们使用针诱导的脑损伤模型来确定 2ccPA 注射对血液凝固和纤溶的影响。2ccPA 抑制血小板脱颗粒相关基因的表达。脑损伤后立即,2ccPA 增加了病变周围 CD41 血小板聚集并促进纤维蛋白聚集。此外,2ccPA 通过上调纤溶酶原激活物的表达来支持纤溶。这些结果表明 2ccPA 对脑止血的急性作用。