新癀片活血化瘀作用机制研究

目的研究新癀片活血化瘀作用的机制。方法采用大鼠体内血栓形成试验、大鼠血瘀模型血流变试验、大鼠血小板聚集试验观察新癀片对血液流变学、血流动力学以及血小板聚集等方面的作用,以及进行肝组织基因芯片检测,研究新癀片活血化瘀作用的机制。结果与对照组比较,新癀片能显著抑制体内血栓形成时间（P〈0.05）,能降低血瘀模型全血黏度及血浆黏度（P〈0.01）,中剂量组显著性更明显（P〈0.001）,能显著抑制血小板聚集（P〈0.001）,基因芯片显示,新癀片各组均显著下调肝组织内皮素转化酶样1蛋白、纤维蛋白原β链、凝固因子Ⅲ、A型内皮素受体、血小板激活因子受体的基因表达。结论新癀片的活血化瘀作用主要是通过减少血小板活化因子受体、凝固因子Ⅲ的基因表达,从而抑制血小板聚集;减少纤维蛋白原表达,改善血浆黏度及延长血栓形成时间;改善红细胞变形能力,抑制红细胞聚集从而改善全血黏度;减少内皮素转化酶样1蛋白、A型内皮素受体基因表达,从而抑制内皮素发挥缩血管活性,改善血流灌注。

Study on mechanism of promoting blood circulation and removing blood stasis of Xinhuang Tablets

Objective To study the mechanism of promoting blood circulation and removing blood stasis of Xinhuang Tablets.Methods Thrombus formation experiment of rats,blood rheological of blood stasis models of rats and platelet aggregation test were used,in order to observe Xinhuang Tablets on hemorheology,haemodynamics and platelet aggregation,and the liver tissue gene chip was detected,the mechanism of promoting blood circulation and removing blood stasis of Xinhuang Tablets was studied.Results Compared with model groups,Xinhuang Tablets could significant inhibit body thrombus formation（P〈0.05）,reduce whole blood viscosity and plasma viscosity（P〈0.05）,middle dose group was significantly more pronounced（P〈0.001）,inhibit platelet aggregation（P〈 0.001）.Gene chips showed Xinhuang Tablets could significantly reduce ET-1,factor Ⅲ,Fg-β chains,ETAR,platelet activating factor receptor gene expression.Conclusion The mechanism of activating blood stasis of Xinhuang Tablets was due to reduce platelet-activating factor receptor,coagulation factors Ⅲ to inhibition of platelet aggregation;reduce expression of fibrinogen to improve plasma viscosity and extension of thrombus formation time;improve red blood cell deformabilityand to inhibit erythrocyte aggregation so as to improve the whole blood viscosity;reduce endothelin converting enzyme-like 1 protein,A-type endothelin receptor gene expression,thereby inhibiting endothelin plays vasoconstrictor activity,improving blood perfusion.