Fig 1: Aspirin inhibits the peripheral blood leukocyte (PBL)–pulmonary microvascular endothelial cell adhesion via the platelet cyclooxygenase 1 (COX-1) but not the cyclooxygenase 2 (COX-2) pathway. A, mRNA expression of platelet COX-1 and COX-2 were measured by real-time polymerase chain reaction. Values are expressed as mean±SEM, 1-way ANOVA, Tukey test, Dahl salt-sensitive (DSS) rat-COX-1: *P=0.005 vs the normal-salt (NS) group, # P=0.030 vs the high-salt (HS) group. Salt-resistant rats (SS13BN) rat-COX-1: # P=0.044 vs HS. B, Serum thromboxane A2 (TXA2) was detected by ELISA kit. Values are expressed as mean±SEM, 1-way ANOVA, Tukey test, DSS rat-TXA2: *P=0.004 vs NS, # P=0.033 vs HS. SS13BN rat-TXA2: # P=0.046 vs HS (C and D). PBL was dyed with 2,7-bis-(2-carboxyethyl)-5 carboxy furancillin acetoxymethyl ester, triflusal was used as the COX-1 inhibitor and lumiracoxib was used as the COX-2 inhibitor, normal salt (133 mmol/L NaCl), high salt (173 mmol/L NaCl), and aspirin (100 µmol/L). The fluorescence signal was captured using a confocal microscope (Leica) and the green fluorescence concentration was proportional to the amount of adhered PBL. Flow cytometry was performed to detect the expression of platelet P-selectin (CD62P+). HS+ASA indicates HS diet with aspirin gavage; PLT, platelet.