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To study the relationship between the inhibiting effect on platelet aggregation and the enhancing effect on epoprostenol (PGI2) released from vascular endothelium with 3,4',5-trihydroxystibene-3-beta-mono-D-glucoside (polydatin, Pol).After having been incubated with Pol, the incubating medium was withdrawn from the bottles with newborn umbilical vein endothelial cells (VEC group, trypsin digesting method) and added to the platelets (washing method). The medium withdrawn from the bottles without VEC was designated as control group. Reduction of platelet aggregation rates (PAR, turbidity method) and changes of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) (radioimmunoassay method) in the supernatant of the aggregated platelets induced by thrombin were scrutinized.PAR in the control group showed no reduction, whereas PAR reduction (-10 +/- 10) and 6-keto-PGF1 alpha increase (108 +/- 30 ng.L(-1)) in the VEC group treated 10 min with Pol 0.41 mmol.L(-1) (vs that of distilled water, ie, 2 +/- 12 and 54 +/- 20 ng.L(-1)) occurred.Increase of PGI2 from VEC by Pol was involved in its (Pol's) inhibition effect of platelet aggregation.

To study the effect of 3,4',5-trihydroxystibene-3-beta-mono-D-glucoside (Polydatin, Pol) on rabbit arterial thrombosis.Rabbit arterial thrombosis was induced by vascular endothelial damage with trypsin.It was showed that the moist weights of the thrombus were 6.6 +/- 1.8 and 4.8 +/- 1.6 mg in Pol 5 and 10 mg.kg-1 groups, respectively, which was lighter than that in control (10.9 +/- 1.9 mg, P0.05, P0.01); the platelet aggregation was inhibited simultaneously. In vitro, Pol 0.30-1.15 mmol.L-1 reduced TXA2 produced in platelets. It did not affect the production of PGI2 in cultured human umbilical vein endothelial cells.Thrombosis was abated by Pol. The selective inhibition of production of TXA2 rather than PGI2, is one of the mechanisms involved.

3,4,5-Trihydroxystibene-3-beta-mono-D-glucoside (PD) from Polygonum cuspidatum 0.05-0.45 mmol/L increased beat rate of myocardial cells from 100% to 112-220%. This action of PD 0.15 mmol/L was agonized by nisoldipine 0.1, propranolol 10 and phentolamine 1 mumol/L. PD (0.05, 0.15 mmol/L) decreased the lactate dehydrogenase (LDH) amount liberated by myocardial cells, from 98 +/- 11 IU/ml of deprivation of oxygen and glucose (DOG) to 55 +/- 16, 68 +/- 14 IU/ml (P less than 0.01) 6 h after injury of DOG; 77 +/- 9, 80 +/- 6 IU/ml (P less than 0.01) 9 h after injury of DOG. PD 0.15 mmol/L decreased the LDH amount liberated by myocardial cells, from 311 +/- 34 to 231 +/- 42 IU/ml (P less than 0.05) 9 h after injury of chlorpromazine (CPZ). It is suggested that PD can protect myocardial cells injured by DOG and CPZ.