Effects of Active Fractions of Danshen or Sanqi on Platelet Adhesion,Aggregation and TXA,PGI in Rat Model of Blood Stasis Syndrome

YANG Jia1; QIN Cai-ling1; Liu Ting1; Zhang Yi1; SUN You-fu1; TAN Hong-gen1; ZHANG Shu-yun1; ZHANG Bo-li2

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Effects of Active Fractions of Danshen or Sanqi on Platelet Adhesion,Aggregation and TXA,PGI in Rat Model of Blood Stasis Syndrome

更新时间：2024-01-04

- Effects of Active Fractions of Danshen or Sanqi on Platelet Adhesion,Aggregation and TXA,PGI in Rat Model of Blood Stasis Syndrome
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 10, Issue 6, Pages: 35-38(2004)
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- Published：2004
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YANG Jia1, QIN Cai-ling1, Liu Ting1, et al. Effects of Active Fractions of Danshen or Sanqi on Platelet Adhesion,Aggregation and TXA,PGI in Rat Model of Blood Stasis Syndrome[J]. Chinese journal of experimental traditional medical formulae, 2004, 10(6): 35-38.
DOI：

YANG Jia1, QIN Cai-ling1, Liu Ting1, et al. Effects of Active Fractions of Danshen or Sanqi on Platelet Adhesion,Aggregation and TXA,PGI in Rat Model of Blood Stasis Syndrome[J]. Chinese journal of experimental traditional medical formulae, 2004, 10(6): 35-38. DOI：

摘要

采用皮下注射肾上腺素加冰水冷浴法造大鼠血瘀模型

观察丹参、三七的有效部位丹酚酸B、Rg对血小板粘聚性及TXB2、6KetoPGF1α的含量的影响。结果表明:大鼠肾上腺素血瘀模型组与正常对照组比较

血浆血小板聚集性(ADP诱导)、粘附性均显著升高

血浆中TXB2、6KetoPGF1α水平及TXB2/6KetoPGF1α比值均无显著影响

对ADP诱导血小板生成的TXB2、腹主动脉组织的6KetoPGF1α的含量及TXB2/6KetoPGF1α比值亦无显著影响。有效部位丹酚酸B、Rg对肾上腺素血瘀模型大鼠血小板粘聚性升高有明显抑制作用。有效部位丹酚酸B、Rg对肾上腺素血瘀模型大鼠血浆中TXB2、ADP诱导血小板生成TXB2及血浆中6KetoPGF1α、腹主动脉组织6KetoPGF1α均有明显升高的作用

对TXB26KetoPGF1α均无明显影响。结论:此血瘀模型复制成功

推测其升高血小板聚集性的机理与TXA2PGI2系统无明显关系。有效部位丹酚酸B、Rg对肾上腺素血瘀模型大鼠血小板粘聚性抑制作用机理推测主要与升高6KetoPGF1α的水平有关。

Abstract

The rat model of blood stasis syndrome was caused by subcutaneous adrenaline injection incorporated with ice-bathing.We studied the effects of the active fractions of Danshen and Sanqi

i.e.salvianolic acid B(Sal.B)and Rg

on platelet aggregation

platelet adhesion

TXA2 and PGI2 in rat model of blood stasis syndromes.The results indicated that compared with normal rats

the platelet adhesion and ADP-induced platelet aggregation were markedly increased.However

the plasma levels of TXB

6-keto-PGF1α and ADP-induced platelet products of TXB2 and 6-keto-PGF1α in abdominal aorta were not markedly affected in the model rats.Sal.B and Rg significantly inhibited the increase in platelet adhesion and ADP-induced platelet aggregation in the model rats.Sal.B and Rg also markedly increased the plasma levels of TXB2

6-keto-PGF1α and ADP-induced platelet production of TXB2 and 6-keto-PGF1α in abdominal aorta of the model

but had little effect on the ratio of TXB2/6-keto-PGF1α.The results indicated that the blood stasis syndrome model was established successfully.We inferred that the changes in platelet aggregation and platelet adhesion might not be related with TXA2-PGI2.Moreover

the other conclusion is that the inhibition effects of Sal.B and Rg of Danshen and Sanqi in Fufangdanshen prescription on platelet aggregation and adhesion might be closely related to its promotive effect on the release of 6-Keto-PGF1α in the rats.

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