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Background {#Sec1} ========== Clinically, ticagrelor and clopidogrel, antiplatelet agglutination agents, are commonly used in combination with percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) \[[@CR1]\]. They cure ACS by targeting the platelet P2Y~12~ adenosine diphosphate (ADP) receptor to inhibit platelet aggregation and reduce thrombosis, and the inhibitory effect of ticagrelor on the P2Y~12~ receptor is reversible, whereas inhibitory effect of clopidogrel is irreversible \[[@CR2]\]. Some studies have indicated that inflammatory cytokines are involved in the initiation and progression of atherosclerosis which is one of the pathological features of ACS \[[@CR3]\]. In addition to triggering thrombus formation at the site of atherosclerotic plaque rupture, platelets also release proinflammatory mediators and interact with other related cells, while antiplatelet therapy can reduce the levels of inflammatory cytokines \[[@CR4]\]. Thus, inflammation plays an important role in ACS. Further research showed that NF-ΚB, a central regulator of inflammation, which is involved in various inflammatory diseases, is associated with susceptibility to ACS \[[@CR4]\]. Furthermore, long-term administration of clopidogrel after severe coronary artery injury reduces inflammation via inhibition of NF-ΚB and activator protein 1 activation in pigs \[[@CR1]\]. There are few reports on the mechanism of P2Y~12~ receptor antagonist-mediated inhibition of inflammation. Therefore, we wanted to know how P2Y~12~ receptor antagonist, including ticagrelor and clopidogrel, can regulate the NF-ΚB signaling pathway and reduce inflammation. In the study, we detected the mRNA levels of related inflammatory factors, the protein level and subcellular localization of molecules in the NF-ΚB signaling pathway, cell viability, apoptosis, the cell cycle, cell migration, and vascular formation, after treating human umbilical vein endothelial cells (HUVECs)stimulated by lipopolysaccharide (LPS) and CD14 with ticagrelor or clopidogrel. Methods {#Sec2} ======= Preliminary experiment {#Sec3} ---------------------- ### Cell proliferation assay {#Sec4} HUVECs (FuHeng Cell Center, Shanghai, China, FH0278) were incubated with ticagrelor (0 μM, 5 μM, 10 μM, 20 μM, 50 μM, 100 μM) clopidogrel (0 μM, 5 μM, 10 μM, 20 μM, 50 μM, 100 μM), separately, for 12 h, 24 h or 48 h. Then cell viability was determined by CCK-8 (Biosharp, BS350B). Formal experiment {#Sec5} ----------------- ### Cell culture and treatment {#Sec6} HUVECs were cultured in complete growth medium that was F12K containing 10% fetal bovine serum (FBS) and 1% Penicillin-Streptomycin Solution at 37 °C with 5% CO~2~. HUVECs were treated with complete growth medium supplemented with DMSO (as control), ticagrelor, clopidogrel, DMSO plus LPS and CD14, ticagrelor plus LPS and CD14, or clopidogrel plus LPS and CD14, separately, for 16 h. The concentrations of these compounds are shown in the Table [1](#Tab1){ref-type="table"}. Table 1The concentrations of these compoundsCompoundsConcentrationsTicagrelor20 μMClopidogrel20 μMLPS10 ng/mLCD141 μg/mL ### Cell proliferation assay {#Sec7} Cells were seeded in 96 well culture plates (2000 cells/well). After the cells were incubated with the indicated compounds for 16 h. Finally, cell viability was tested with CCK8 reagent. We evaluated cell viability by measured the absorbance at 450 nm. ### Western blot assay {#Sec8} Whole cell extracts were lysed in RIPA Lysis buffer (Beyotime, P0013B) containing 1 mM phenylmethylsulfonyl fluoride (PMSF). Then protein concentration of