AIM: 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). METHODS: After having been incubated with Pol, the incubating medium was withdrawn from the bottles with newborn umbilical vein endothelial cells (VEC group, trypsin digesting method) and added to the platelets (washing method). The medium withdrawn from the bottles without VEC was designated as control group.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. RESULTS: 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. CONCLUSION: Increase of PGI2 from VEC by Pol was involved in its (Pol's) inhibition effect of platelet aggregation.
AIM: 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). METHODS: After having been incubated with Pol, the incubating medium was withdrawn from the bottles with newborn umbilical vein endothelial cells (VEC group, trypsin digesting method) and added to the platelets (washing method). The medium withdrawn from the bottles without VEC was designated as control group.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. RESULTS: 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. CONCLUSION: Increase of PGI2 from VEC by Pol was involved in its (Pol's) inhibition effect of platelet aggregation.