Objective: To explore the protective effect of tanshinone Ⅱ A on lipopolysaccharide (LPS)-induced lung injury in rats, and possible mechanism. Methods: LPS (O111: B4) was used to produce a rat model of acute lung injury. Sprague-Dawley rats were randomly divided into 3 groups (8 in each group): the control group, the model group (ALl group), and the tanshinone ⅡA treatment group. Expression of adhesion molecule CD18 on the surface of polymorphonuclear neutrophil (PMN-CD18) in venous white blood cells (WBC), and changes in coagulation-anticoagulant indexes were measured 6 h after injection of LPS or normal saline. Changes in malondialdehyde (MDA) content, wet and dry weight (W/D) ratio and morphometry of pulmonary tissue as well as PMN sequestration in the lung were also measured. Results: (1) When compared with the control group, expression of PMN-CD18 and MDA content were enhanced in the ALl group with a hypercoagulable state (all P＜0.01) and an increased W/D ratio (P＜0.05). Histopathological morphometry in the lung tissue showed higher PMN sequestration, wider alveolar septa; and lower alveolar volume density (Vv) and alveolar surface density (Sv), showing significant difference (P＜0.01). (2) When compared with the ALl group, the expression of PMN-CD18, MDA content, and W/D ratio were all lower in Tanshinone ⅡA treatment group (P＜0.05)with ameliorated coagulation abnormality (P＜0.01). Histopathological morphometry in the lung tissue showed a decrease in the PMN sequestration and the width of alveolar septa (both P＜0.01), and an increase in the Vv and Sv (P＜0.05, P＜0.01). Conclusion: Tan ⅡA plays a protective role in LPS-induced lung injury in rats through improving hypercoagulating state, decreasing PMN-CD18 expression and alleviating migration, reducing lipid peroxidation and alleviating pathological changes.