The preliminary study on the antithrombotic mechanism of glycosaminoglycan from mactra veneriformis.

The effect of glycosaminoglycan from Mactra veneriformis on deep venous thrombosis of rats was observed, and the preliminary antithrombotic mechanism of glycosaminoglycan was explained. The results showed that when the glycosaminoglycan was injected intravenously into rats within the dose range of 0.0313-1 mg/kg, the antithrombotic effect increased as the dose increased. When the dose was increased to and exceeded 0.125 mg/kg, deep venous thrombosis caused by blood stagnation was inhibited significantly or extremely remarkably (P < 0.05, P < 0.01), while the intensity was similar to that of the tool drug heparin sodium at the same dose and weaker than that of heparin calcium of low molecular weight at three times' dose in clinics. Three doses (0.1, 0.4 and 1.6 mg/kg) of glycosaminoglycan were intravenously injected via mice tail, resulting in an extremely significant increase of activated partial thromboplastin time (APTT) and thrombin time (TT) (P < 0.01), no significant change of prothrombin time (PT) (P > 0.05), and a weaker anticoagulant effect than that of heparin sodium. In-vitro experiments demonstrated that except for the 2 μg/ml of glycosaminoglycan (P > 0.05), other final concentration groups significantly or extremely significantly prolonged the APPT, TT and PT of rabbits (P < 0.05, P < 0.01), but with a slightly weaker anticoagulant effect than that of heparin sodium; The antiplatelet aggregation experiments using big-eared rabbits manifested that glycosaminoglycan markedly decreased the maximum aggregation percentage of rabbits blood platelet (P < 0.01), which indicated that it had good antiplatelet aggregation effect, but the intensity was weaker than the positive control drug, Ozagrel sodium.