Hydroxysafflor Yellow A suppresses thrombin generation and inflammatory responses following focal cerebral ischemia-reperfusion in rats
Hydroxysafflor Yellow A suppresses thrombin generation and inflammatory responses following focal cerebral ischemia-reperfusion in rats
复制标题
Hydroxysafflor Yellow A 可抑制大鼠局灶性脑缺血再灌注后凝血酶的生成和炎症反应。
DOI：
10.1016/j.bmcl.2010.05.076
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发表时间：
2010-07-15
影响因子：
2.7
通讯作者：
Zhang, Xiumei
中科院分区：
文献类型：
--
作者：
Sun, Xia;Wei, Xinbing;Zhang, Xiumei
羟基喜树碱黄A已被证明可以减轻大鼠的压力超负荷肥大，并抑制血小板聚集。本研究发现，羟基红花黄色素A可通过抑制凝血酶的生成来预防脑缺血再灌注损伤。此外，用羟基茴香醚黄A处理显著抑制NF-κ B B p65核翻译和p65结合活性、ICAM-1的mRNA和蛋白水平以及中性粒细胞的浸润。同时，羟丙基黄色素A能改善神经功能缺损评分，增加海马CA 1区存活锥体细胞数，降低血浆血管紧张素II水平。结果提示，羟基红花黄色素A抗脑缺血的机制可能与其抑制凝血酶生成，降低血管紧张素II含量，从而抑制凝血酶诱导的炎症反应有关。(C)2010年由Elsevier Ltd.出版
Hydroxysafflor Yellow A has been demonstrated to attenuate pressure overloaded hypertrophy in rats and inhibit platelet aggregation. Herein we found that Hydroxysafflor Yellow A prevented cerebral ischemia-reperfusion injury by inhibition of thrombin generation. In addition, treatment with Hydroxysafflor Yellow A significantly inhibited NF-kappa B p65 nuclear translation and p65 binding activity, both mRNA and protein levels of ICAM-1 and the infiltration of neutrophils. Mean while, Hydroxysafflor Yellow A had the capacity to improve neurological deficit scores, increase the number of the surviving hippocampal CA1 pyramidal cells and decrease the plasma angiotensin II level. These results illustrated that anti-cerebral ischemic mechanism of Hydroxysafflor Yellow A may be due to its suppression of thrombin generation and inhibition of thrombin-induced inflammatory responses by reducing angiotensin II content. (C) 2010 Published by Elsevier Ltd.