Abstract:
AIM To investigate the effect of biophotin on platelet function induced by the combined use of aspirin and clopidogrel.
METHODS Human platelets were used for the research. Platelet injury was induced by combined use of aspirin and clopidogrel. Platelets were divided into control group, model group and biophotin group. Platelet activation marker CD62P was detected by flow cytometry, platelet aggregation was measured by impedance method, platelet adhesion on fibrinogen was assessed by immunofluorescence and the levels of CD62P and platelet activating factor (PAF) in platelets were measured by enzyme-linked immunosorbent assay.
RESULTS Compared with the control group, the model group showed decreased surface activation of CD62P, inhibited platelet aggregation and adhesion and reduced levels of CD62P and PAF in platelets (all P<0.01). Compared with the model group, the biophotin group showed enhanced surface activation of CD62P (P<0.05), increased platelet aggregation (P<0.05, P<0.01) and adhesion (P<0.01) and higher levels of CD62P and PAF in platelets(P<0.05).
CONCLUSION Biophotin alleviates platelet dysfunction induced by combined aspirin and clopidogrel, and it may help reduce the bleeding risk in patients on long-term antiplatelet therapy during trauma and perioperative periods.