Refined Qing Kai Ling, traditional Chinese medicinal preparation, reduces ischemic stroke-induced infarct size and neurological deficits and increases expression of endothelial nitric oxide synthase
Refined Qing Kai Ling, traditional Chinese medicinal preparation, reduces ischemic stroke-induced infarct size and neurological deficits and increases expression of endothelial nitric oxide synthase
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精制清开灵是一种传统中药制剂，可减少缺血性中风引起的梗塞面积和神经功能缺损，并增加内皮一氧化氮合酶的表达。
DOI：
10.1248/bpb.31.633
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发表时间：
2008-04-01
影响因子：
2
通讯作者：
Shen, Yong
中科院分区：
文献类型：
--
作者：
Hua, Qian;Zhu, Xiaolei;Shen, Yong
精制清开灵（RQKL）是从清开灵中提取的多组分注射剂，通过减轻血管内皮细胞的损伤，抑制炎症过程，对大鼠大脑中动脉闭塞（MCAO）模型具有神经保护作用。本实验观察了RQKL对内皮型一氧化氮合酶（eNOS）表达的影响，并探讨其对缺血再灌注损伤的保护作用机制。采用永久性线栓法建立大鼠大脑中动脉缺血模型。结果表明，RQKL能明显缩小模型大鼠的脑梗死面积，改善神经功能缺损程度。此外，还显示，在永久性MCAO后2至72 h，缺血半暗带血管内皮中的eNOS水平持续增加，并且在用RQKL治疗的动物中eNOS的表达增加更多。结果提示：大鼠局灶性脑缺血后半暗带eNOS表达增强，RQKL可刺激缺血后eNOS表达，这可能是RQKL抗脑缺血的重要机制。
Refined Qing Kai Ling (RQKL) is an improved injectable multi-component preparation derived from Qing Kai Ling, which could offer the neuroprotection effect in middle cerebral artery occlusion (MCAO) model of rats by relieving the damage of vascular endothelial cell as well as inhibiting the process of inflammation. Herein, we observed whether RQKL could exert influence on the expression of endothelial nitric oxide synthase (eNOS), as a mechanism of its protective effects against ischemia. Sprague-Dawley rat model of focal cerebral ischemia was established by permanent filament occlusion of the left middle cerebral artery. We found that the administration of RQKL could reduce the ischemic infarct size as well as neurological deficit of model rats. Furthermore, it was showed that the eNOS level was consistently increased in endothelium of blood vessels of the ischemic penumbra after 2 to 72 h of permanent MCAO, and the expression of eNOS increases more in animals treated with RQKL. Our results suggested that eNOS levels in penumbral zone were enhanced after permanent focal ischemia, and RQKL could stimulate postischemic eNOS expression, which may be an important mechanism in RQKL's protection against cerebral ischemia.