Figure 2
Figure 2. L5-induced platelet aggregation and adhesion. The results of platelet aggregation detected by using an aggregometer are shown. (A) Compared with the PBS control, 50 µg/mL L1 or L5 alone induced no platelet aggregation. (B) ADP-induced platelet aggregation was enhanced by the addition of 5, 25, or 50 µg/mL L5 in a dose-dependent manner. The quantification of aggregation is shown as the ratio of the treated group to the ADP-treated control (Ctl). Data are presented as the mean ± standard deviation (n = 6). *P < .05; **P < .01 vs ADP-treated control, determined by using 1-way analysis of variance with the Bonferroni post hoc test. (C) Parallel plate flow chamber analysis showed that platelets treated with 50 µg/mL L5 adhered to the fibrinogen-coated bottom of the chamber at a flow rate of 1500 S−1 (n = 3), whereas those treated with 50 µg/mL L1 or PBS (Ctl) did not.

L5-induced platelet aggregation and adhesion. The results of platelet aggregation detected by using an aggregometer are shown. (A) Compared with the PBS control, 50 µg/mL L1 or L5 alone induced no platelet aggregation. (B) ADP-induced platelet aggregation was enhanced by the addition of 5, 25, or 50 µg/mL L5 in a dose-dependent manner. The quantification of aggregation is shown as the ratio of the treated group to the ADP-treated control (Ctl). Data are presented as the mean ± standard deviation (n = 6). *P < .05; **P < .01 vs ADP-treated control, determined by using 1-way analysis of variance with the Bonferroni post hoc test. (C) Parallel plate flow chamber analysis showed that platelets treated with 50 µg/mL L5 adhered to the fibrinogen-coated bottom of the chamber at a flow rate of 1500 S−1 (n = 3), whereas those treated with 50 µg/mL L1 or PBS (Ctl) did not.

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