In the current study, SCH530348 blocked PAR-1 signaling and thrombin/PAR-1 interaction during lung IR injury, subsequently suppressed PI3K/Akt, MAPK, and NF-κB signaling activation, prevented neutrophil recruitment, and decreased downstream proinflammatory cytokine production, including TNF-α, IL-6 and CINC-1. This evidence concerns the gene AKT1 and medical procedure.