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. 2009 Oct 8;158(6):1548–1556. doi: 10.1111/j.1476-5381.2009.00440.x

Table 2.

Effect of several inhibitors on thrombin-, PAR1-AP- and PAR4-AP-induced platelet aggregation (% ± SEM)

Control DMSO0.2% U73122 10 µM LY294002 50 µM Ro31-8220 10 µM PP2 10 µM Staurosporine 1 µM
Thrombin 0.2 U·mL−1 83.3 ± 1.7 1.2 ± 0.2* 48.2 ± 7.9* 5.6 ± 0.8* 48.8 ± 6.7* 13.8 ± 3.5*
PAR1-AP 25 µM 78.3 ± 0.8 0.8 ± 0.1* 37.9 ± 2.9* 8.9 ± 2.4* 45.6 ± 4.3* 5.9 ± 0.5*
PAR4-AP 150 µM 85.5 ± 2.1 0.9 ± 0.2* 46.4 ± 8.3* 1.0 ± 0.2* 73.3 ± 5.0 5.8 ± 0.7*

Washed platelets were stimulated with thrombin, PAR1-AP or PAR4-AP in the absence or presence of the phospholipase C inhibitor U73122, PI3K inhibitor LY294002, protein kinase C inhibitor Ro 31-8220, Src kinase inhibitor PP2 and the broad spectrum inhibitor of protein kinases staurosporine, and aggregation was recorded as described in Methods. Data were derived from four different experiments.

*

P < 0.05 versus control activated samples.