“…Magnolia compounds have been known for more than 20 years to interfere in some major pathways of platelet activation/inhibition: (1) TBXs, some of the most powerful agonists for platelet activation and major contributors to thrombus formation; TXB2, whether induced by collagen, arachidonic acid, or thrombin, is inhibited by magnolol and honokiol; also five aporphine alkaloids isolated from leaves of M. obovata, N-acetylanonaine, N-acetylxylopine, Nformylanonaine, liriodenine, and lanuginosine, show potent antiplatelet activities, probably by interfering with TXA2 production and/or binding (Teng et al, 1988;Pyo et al, 2003;Ho and Hong, 2012); (2) the activation of PPAR isoforms (α, β/δ, and γ), a pathway known to inhibit platelet aggregation; magnolol (20-60 μmol/L) dose-dependently enhances the activity and intracellular level of PPAR-β/γ in platelets (Shih and Chou, 2012); and (3) the cytosolic Ca 2+ influx and/or mobilization from intracellular stores that plays a crucial role in the platelet responses to various agonists (Lee et al, 2011); the rise of intracellular calcium caused by arachidonic acid or collagen is suppressed by both magnolol and honokiol (Teng et al, 1988;Pyo et al, 2003;Lee et al, 2011).…”