HMGB1 and acute respiratory distress syndrome: HMGB1 plays a critical role in mediating hyperoxia induced ALI through the recruitment of leukocytes into the lung [58], a single dose of EP treatment (40 mg/kg intraperitoneal injection prior to hyperoxia exposure, and lung tissue samples were taken 24 h after hyperoxia exposure) attenuates the hyperoxia induced ALI probably by inhibiting HMGB1 secretion from hyperoxic macrophages [58], suggesting that EP may treat oxidative inflammatory lung injury in patients receiving hyperoxia through mechanical ventilation.