Figure 5
Figure 5. Mediation of the L5-induced signaling pathway by PAFR and LOX-1. Phosphorylation of (A) PKCα, (B) PI3K, and (C) Akt induced by the combination of 4 μM ADP and 25 μg/mL L5 was prevented by ABT-491 (blocks PAFR), TS-92 (neutralizes LOX-1), Wortmannin (Wort; inhibits PI3K), and RO318820 (inhibits PKC activation). The expression of protein is shown as a ratio to that of the PBS-treated control (Ctl) group. (D) Platelet aggregation induced by ADP and 25 μg/mL L5 was attenuated in the presence of ABT-481, TS-92, Wortmannin, and RO318820. Black bars represent the mean ± standard deviation. *P < .05; **P < .01 vs ADP + L5-treated group (n = 5), determined by using 2-way analysis of variance with the Bonferroni post hoc test.

Mediation of the L5-induced signaling pathway by PAFR and LOX-1. Phosphorylation of (A) PKCα, (B) PI3K, and (C) Akt induced by the combination of 4 μM ADP and 25 μg/mL L5 was prevented by ABT-491 (blocks PAFR), TS-92 (neutralizes LOX-1), Wortmannin (Wort; inhibits PI3K), and RO318820 (inhibits PKC activation). The expression of protein is shown as a ratio to that of the PBS-treated control (Ctl) group. (D) Platelet aggregation induced by ADP and 25 μg/mL L5 was attenuated in the presence of ABT-481, TS-92, Wortmannin, and RO318820. Black bars represent the mean ± standard deviation. *P < .05; **P < .01 vs ADP + L5-treated group (n = 5), determined by using 2-way analysis of variance with the Bonferroni post hoc test.

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