Sulforaphane attenuates glycoprotein VI-mediated platelet mitochondrial dysfunction through up-regulating the cAMP/PKA signaling pathway <i>in vitro</i> and <i>in vivo</i>
Xinyu Zhou, Xinhui Huang, Chunting Wu, Yongjie Ma, Weiqi Li, Jinqiu Hu, Rong Li, Fuli Ya
Abstract
. Mechanistically, these inhibitory effects of SFN treatment and BSE supplementation were mainly mediated by up-regulating the cAMP/PKA pathway though decreasing phosphodiesterase 3A (PDE3A) activity. Thus, through modulating the PDE3A/cAMP/PKA signaling pathway, and attenuating platelet mitochondrial dysfunction and hyperreactivity, SFN may be a potent cardioprotective agent.
Topics & Concepts
In vitroChemistryIn vivoSulforaphanePharmacologyCell biologySignal transductionBiochemistryBiologyBiotechnologyGenomics, phytochemicals, and oxidative stressMast cells and histamineCoagulation, Bradykinin, Polyphosphates, and Angioedema