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首页> 外文期刊>Experimental Neurology >LAU-0901, a novel platelet-activating factor antagonist, is highly neuroprotective in cerebral ischemia.
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LAU-0901, a novel platelet-activating factor antagonist, is highly neuroprotective in cerebral ischemia.

机译：LAU-0901是一种新型的血小板活化因子拮抗剂，在脑缺血中具有高度的神经保护作用。

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Platelet-activating factor (PAF) is a bioactive phospholipid that accumulates during ischemia-reperfusion and is involved in the activation of platelets, neutrophils, and pro-inflammatory signaling. PAF has been suggested to enhance brain ischemia-reperfusion damage. LAU-0901, a novel PAF receptor antagonist, was examined in models of focal cerebral ischemia in rats and mice. Sprague-Dawley rats were anesthetized and received 2-hour middle cerebral artery occlusion (MCAo) by intraluminal suture. LAU-0901 (30, 60, 90 mg/kg; n=9-11) or vehicle (n=11) was administered i.p. at 2 h after onset of MCAo. The neurological status was evaluated at 60 min, and on days 1, 2, 3 and 7 after MCAo. In the dose-response study in mice, C57BL/6 mice were anesthetized and received 1 h MCAo by intraluminal suture. LAU-0901 (15, 30, 60 mg/kg; n=7-9) or vehicle (n=8) was given i.p. at 1 h after onset of MCAo. Local cerebral blood flow (LCBF) was measured at 1, 2, 4, and 6 h after MCAo in mice. LAU-0901 treated rats showed improved neurological score throughout the 7-day survival period. LAU-0901 treatment (30, 60 and 90 mg/kg) reduced total corrected infarct volume compared to vehicle rats by 76, 88 and 90%, respectively. Mice treated with LAU-0901 (30 and 60 mg/kg) reduced total infarction by 29% and 66%, respectively. LCBF was improved by treatment with LAU-0901 (30 mg/kg) by 77% of baseline at 6 h. In conclusion, we demonstrate for the first time that LAU-0901 improves behavioral scores, LCBF and reduces infarct volume after focal cerebral ischemia in rats and mice. Thus, this PAF receptor antagonist exhibits potent and sustained neuroprotection that may be of value for the design of stroke therapies.
机译：血小板激活因子（PAF）是一种生物活性磷脂，在缺血再灌注过程中积累，并参与血小板，嗜中性粒细胞和促炎信号的激活。已经提出PAF可增强脑缺血-再灌注损伤。在大鼠和小鼠的局灶性脑缺血模型中检查了一种新型的PAF受体拮抗剂LAU-0901。麻醉Sprague-Dawley大鼠，并通过腔内缝合法接受2小时的大脑中动脉闭塞（MCAo）。腹膜内给予LAU-0901（30、60、90 mg / kg; n = 9-11）或赋形剂（n = 11）。在MCAo发作后2小时内。在MCAo后60分钟以及第1、2、3和7天评估神经系统状况。在小鼠的剂量反应研究中，麻醉C57BL / 6小鼠并通过腔内缝合法接受1 h MCAo。腹膜内给予LAU-0901（15、30、60 mg / kg; n = 7-9）或赋形剂（n = 8）。在MCAo发作后1小时。在小鼠MCAo后1、2、4和6小时测量局部脑血流量（LCBF）。 LAU-0901处理的大鼠在整个7天的生存期内均显示出改善的神经学评分。与媒介物大鼠相比，LAU-0901治疗（30、60和90 mg / kg）分别使总纠正梗死体积减少了76％，88％和90％。用LAU-0901（30和60 mg / kg）治疗的小鼠分别将总梗死减少了29％和66％。通过在6 h时用LAU-0901（30 mg / kg）治疗，可改善LCBF基线水平的77％。总之，我们首次证明LAU-0901可改善大鼠和小鼠局灶性脑缺血后的行为评分，LCBF并减少梗塞体积。因此，该PAF受体拮抗剂表现出有效和持续的神经保护作用，这对中风疗法的设计可能具有价值。

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