Galla rhois exerts its antiplatelet effect by suppressing ERK1/2 and PLCβ phosphorylation

- Galla rhois extract showed a possibility of the antiplatelet activity.
- Galla rhois extract suppressed ERK1/2 phosphorylation and PLCβ phosphorylation.
- Galla rhois extract includes MG and PGG, as its components.
- Methyl gallate (MG) inhibited the collagen-induced platelet activation.
- Penta-O-galloyl-β-d-glucoside (PGG) inhibited thrombin-induced platelet activation.

Galla rhois and its components have various biological activities, including protective effects on liver cells as well as antimetastatic, antiplatelet, and antibacterial effects. In the present study, we identified the antiplatelet activity and possible mechanism of action of a G. rhois extract (GRE). We investigated the effect of GRE and its components on rabbit platelet activation, and their possible molecular mechanisms. The GRE inhibited collagen-, AA-, and thrombin-induced platelet aggregation as well as serotonin secretion, in a concentration-dependent manner. The GRE significantly inhibited the production of lipoxygenase-mediated 12-hydroxyeicosatetraenoic acid. The GRE effectively suppressed thrombin-stimulated PLCβ3 phosphorylation and collagen-induced ERK1/2 phosphorylation, in addition, the GRE significantly restored the cAMP level, which had decreased due to collagen or thrombin. Among the components of GRE, methyl gallate inhibited the collagen-induced platelet activation through suppression of ERK phosphorylation, penta-O-galloyl-β-d-glucoside inhibited the thrombin-induced platelet activation through suppression of PLCβ phosphorylation.These results indicate that the GRE including methyl gallate and penta-O-galloyl-β-d-glucoside suppressed platelet activation by inhibiting ERK1/2 and PLCβ3 phosphorylation.