Effects Of Ginkgo Biloba Extract And Aspirin On The Production Of Ros And The Expressions Of LOX-1and Phosphorylation P38MAPK In Human Coronary Artery Endothelial Cells Induced By Activated Platelets

Aim: In the present study, we investigated whether the therapeutic dosages of Ginkgo biloba Extract (EGb) and Aspirin, especially in combination, might synergistically suppress oxidative stress through regulating the expression of LOX‐1and phosphorylation of p38MAPK in human coronary artery endothelial cells (HCAECs) induced by activated platelets ex vivo.Methods: HCAECs were stressed with2×108/ml activated platelets and followed by Aspirin (1,2or5mmol/L), EGb (4,40or400μg/ml) and combinational (1mmol/L Aspirin and40μg/ml EGb) treatments in three groups for12hours. Superoxide anion in HCAECs was measured with H2DCF‐DA probe. The expression of LOX‐1and phosphorylated p38MAPK were examined by Western Blot.Results: After stimulation of activated platelets, intracellular superoxide anion was increased about3folds in HCAECs (p<0.05vs. control). Both Aspirin and EGb reduced superoxide anion in HCAECs in a dosage dependent manner (p<0.05vs. activated platelets). Combinational administration of Aspirin and EGb showed synergistic effect (p<0.05vs. aspirin or EGb alone). By Western blot analysis, after stimulation of activated platelets, we were able to show that activated platelets markedly enhanced the expression of LOX‐1and phosphorylation of p38MAPK (p<0.05vs. control). Both Aspirin and EGb only inhibited LOX‐1expression in a dosage dependent manner (p<0.05vs. activated platelets), but not p38MAPK phosphorylation. As expected, the combination of Aspirin and EGb markedly reduced not only the expression of LOX‐1and but also the p38phosphorylation (p<0.05vs. aspirin or EGb alone).Conclusions: Both EGb and Aspirin attenuate the oxidative stress of HCAECs stimulated by activated platelets ex vivo. It appears that the synergistic effects of EGb and Aspirin may correlate with the inhibition of ROS production, LOX‐1expression and p38MAPK phosphorylation. The underlying protection mechanisms of EGb, aspirin, and their combination against atherosclerosis may correlate with the inhibition of ROS production and LOX‐1and p‐p38expression.