AIM: To investigate the inhibiting effect and mechanism of dimethylaminoethyl ginkgolide B mesylate on platelet aggregation and release function.METHODS: The effect of dimethylaminoethyl ginkgolide B mesylate on inhibiting PAF-induced platelet aggregation was measured by turbidimetry method through giving rabbits dimethylaminoethyl ginkgolide B mesylate at different final concentration via i.v.for 5 days.The release of Ca2 + from PAF-induced platelet in rabbits was assayed with fluorospectrophotometry and the contents of TXA2 and PGI2 were measured by radio-immunity method.RESULTS: Three groups of dimethylaminoethyl ginkgolide B mesylate (1.95,3.90,7.80 mg/kg) had significant effect on inhibiting PAF-induced platelet aggregation in rabbits (compared to normal,P

Objective To observe the effect of ginkolide B derivative(XQ) on animal thrombosis.Methods SD male rats were randomized into the model group,troxerutin(48 mg?kg-1?d-1) group,ginkolide B(7.8 mg?kg-1?d-1) group,and low-,middle-and high-dose XQ(in the dose of 3.9,7.8 and 15.6 mg?kg-1?d-1 respectively) groups.The anti-thrombotic effect of XQ was observed on rats mixed thrombosis model induced by arterio-venous shunt method and electrical stimulation.Meanwhile,ICR male mice were randomized into the model group,troxerutin(96 mg?kg-1?d-1) group,ginkolide B(15.6 mg?kg-1?d-1) group,and low-,middle-and high-dose XQ(in the dose of 7.8,15.6 and 31.2 mg?kg-1?d-1 respectively) groups.The anti-thrombotic effect of XQ was also observed on mice acute pulmonary embolism model induced by adenosine diphosphate(ADP).Results XQ at the dose of 7.8 and 15.6 mg?kg-1?d-1 decreased the dry and wet weight of the thrombosis,and obviously prolonged the formation time of rats carotid artery thrombosis as compared to the model group(P

AIM:To compare the effects of atorvastatin at different doses on the function of endothelial proge-nitor cells (EPCs) in the patients with ST-segment elevation myocardial infarction (STEMI).METHODS:The patients of STEMI (n=40) were chosen.According to treatment with different doses of atorvastatin calcium tablet, they were randomly divided into a group of 20 mg and a group of 40 mg (20 cases in each group).The EPCs isolated from the patients were identified and quantitatively analyzed at different time points (before the treatment and on days 5, 10, 15, 20, 30, 60, 90 and 120 after the treatment) by flow cytometry.The surface markers of the EPCs, CXC chemokine receptor 4 (CXCR4), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and silent information regulator 1 (SIRT1), were also detected.RESULTS:On the 5th day, the group of 40 mg demonstrated stronger cell proliferation capability and higher expression levels of CXCR4, VEGF and bFGF than the group of 20 mg (P<0.05).From the 10th day to 120th day, the group of 20 mg revealed stronger cell proliferation capability and higher expression levels of CXCR4, VEGF and bFGF than the group of 40 mg (P<0.05).Within 30 d, the expression of SIRT1 showed no significant diffe-rence between the 2 groups, yet it witnessed a marked change after that and peaked on the 60th day with a drop afterwards.At each time point, the SIRT1 expression level in the group 20 mg was observed higher than that in the group of 40 mg (P<0.05).CONCLUSION:In the acute phase, the repair function of the body treated with atorvastatin at dose of 40 mg is better than that with 20 mg.However, in a long term the low concentration of statin therapy works better in improving the vascular intima and promoting the angiogenesis than high concentration.