Patients with paditaxel-eluting stents are concerned with stent duumbosis caused by Premature discontinLidtion of dual antiplatelet therapy or clopiclogrel resistance. 1 his Study investigatcS thc affect of i epiga I locatechin-31-ga I late (ECCC) oil the expression of throml)jnf'paclitaxel-in(iticoct criclothelial tissue factor CHI) expressions in human aortic enclothelial cells (HAFCs). EGCG was nontoxic to IiAFC% it 0 h LIP to a I- oncentration of 25 [unol/L. At a concentration of 25 pmol/L, FGCG pretrem nirrit potently iill I).ted both thrombin-stimulated and thionibjiill)aclitaxel-StillILIlate(I endothelial TF picituin expression. Thrombin and thrombi n/pacl itaxel-i nduced 2.6--fold and 2.9-fold increases in TF a(tivity compared vvith the contiol EGCG pretreatment caused a 29'-.' arid 38` decrease in ffactivity oil throinbin aod thioni:)m/ paclitaxel treatment. respectively. Real-time polyrnerase chain reaction (11CIR) showed that thrombin and thrombin/paclitaxel-induced 3.0-fold and 46 fold TF mRNA expressions compared wit:i the connul. EGCG pretreatment CdUsed an 82% and 7).: decrease in TF mRNA expression on thrombin arid thrombin/paclitaxel treatment, iespectively The C-ILm terminal N112 lanase (.INK) inhibitor SP600125 wducM till 0111I)III/PaditaXel-IlIdUced TF expression Furthermore, EGCG significantly inhibned the -ollosphorylation ofJNK to49% ofthrornbin/paclitaxel stimulated HAECs ar GO min. Immunol'ILlonscenc-assay did not show in inhibitory effect of EGCC on P65 NF-KB nuclear translocation in the thl'Ollli)lil/l)aL'Iitaxel-st;iiiulated endothelidl cells In conclusion, EGCG call inhibit TF expression in ffil-Ollibill/PaLlitaXel stinlill'ited enclothelial cells via the inhibition ofJNK phosphorylation. The unique property of EC.CG may be LISed to develop d new drug-ell-Iting stent by co-coatin.- FGCG arid paclitaxel. 2009 Elsevier In(- All rights ieseived.