Sulforaphane attenuates glycoprotein VI-mediated platelet mitochondrial dysfunction through up-regulating the cAMP/PKA signaling pathway in vitro and in vivo

Treatment of SFN in human platelets or 12-week supplementation of SFN-enriched BSE in mice attenuates GPVI-mediated mitochondrial dysfunction, apoptosis and activation, which depends on decreasing PDE3A activity and up-regulation of the cAMP/PKA pathway.