Can Isoquinoline Alkaloids Affect Platelet Aggregation in Whole Human Blood?

Figures

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  Figure 1. Structures of studied isoquinoline alkaloids.

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  Figure 2. Antiplatelet effect against platelet aggregation triggered by arachidonic acid. (A) Comparison at a final concentration of 80 μM. (B) Concentration-dependent curves of the active compounds. The colors correspond with part (A) of this figure. Compounds with black columns were inactive (vs. DMSO, the negative control). * p < 0.05 vs. ASA (acetylsalicylic acid, positive control); *** p < 0.001 vs. ASA; ++ p < 0.05 vs. papaverine; +++ p < 0.001 vs. papaverine.

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  Figure 3. Effect of active alkaloids on collagen-triggered platelet aggregation. (A) Comparison of active alkaloids at a concentration of 80 μM. (B) Concentration-dependent curves of the most active compounds. ** p < 0.01 vs. the negative control (DMSO); *** p < 0.01 vs. DMSO; + p < 0.05 vs. ASA (acetylsalicylic acid); +++ p < 0.001 vs. ASA; # p < 0.05 vs. papaverine; ### p < 0.001 vs. papaverine.

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  Figure 4. Antiplatelet effect of papaverine and bulbocapnine on thromboxane analog U46619-induced aggregation. Whole human blood was incubated with a solvent (DMSO) or different concentrations of tested compounds. U46619 at a final concentration of 130 nM was then added to induce the platelet aggregation.

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  Figure 5. Effect of the tested compounds on blood coagulation. Comparison of activated partial thromboplastin time (aPTT) values (A) and prothrombin time (PT) values (B) of tested compounds at a final concentration of 100 μM. DMSO was used as a vehicle at a final concentration of 1% and heparin was used as a positive control at final concentrations of 5 IU/mL and 0.5 IU/mL for PT and aPTT tests, respectively. *** p < 0.001 vs. solvent (DMSO).