Abstract: Objective To study the inhibitory effect of ginkgolide B (GB) on platelet activation as well as on the interaction between platelets and colorectal cancer HCT-116 cells. Methods Whole blood or platelets were treated with different concentrations of GB (5, 15, 30 μmol/L). Thromboelastogram (TEG) , then platelet Adenosine diphosphate was detected . The inhibitory rate of ADP and arachidonic acid (AA) pathway was detected by flow cytometry. The effects of GB on the expression of CD62P and PAC-1 after thrombin and ADP-activated platelets were detected. The effect of GB on the cell migration of platelets and HCT-116 cells after 24 and 48 h interaction was observed by cell scratch test, and the effect of GB on the adhesion of platelets to HCT-116 cells was observed by cell adhesion test. Results (1) TEG test results showed that with the increase of GB concentration, AA inhibition rates increased significantly in dose-dependent manner (P<0.001), the difference was statistically significant compared with the control group (P<0.001); The inhibition rate of ADP in the drug group was significantly increased compared with the control group in a dose-dependent manner (P<0.001), the differences were statistically significant (P<0.001). (2) Flow cytometry showed that after thrombin and ADP activated platelets, the positive rates of CD62P and PAC-1 in the drug group decreased with the increase of drug concentration in a dose-dependent manner (P<0.001), the positive rate of PAC-1 in 5 µmol/L group with thrombin activation pathway was lower than that in control group, and the difference was not statistically significant (P<0.05), the positive rate of CD62P in 5 µmol/L group, the positive rate of PAC-1 in 5µmol/L and 15µmol/L groups of ADP-activated pathway drugs was lower than that of control group, and the difference was not statistically significant (P<0.05), and there were statistically significant differences between the remaining concentration groups and the control group (P<0.01). (3) Scratch test results showed that 24 and 48 h cell mobility in different concentration groups was lower than that in thrombin group and ADP group, respectively, and the difference was statistically significant (P<0.01), cell mobility at 24 and 48 h in 15µmol/L group was significantly lower than that in 5 µmol/L group, and the difference was statistically significant (P<0.05), the mobility of 30 µmol/L group was lower than that of 15 µmol/L group, but the difference was not statistically significant (P<0.05). (4) The adhesion test results showed that activated platelets could enhance the adhesion between them and tumor cells, but the adhesion rate of all groups in the drug group was lower than that in the positive group, and the adhesion rate decreased with the increase of drug concentration. Conclusion GB can inhibit platelet activation through AA pathway and ADP pathway, and then inhibit the adhesion of platelets to HCT-116 tumor cells and promote the migration of tumor cells.

Key words: Ginkgolide B, Colorecta l cancer, Platelets, Adhesion, Migration