To explore the protective effect of tanshinone II A on lipopolysaccharide (LPS)-induced lung injury in rats

and possible mechanism. 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 (ALI group)

and the tanshinone II A treatment group. Expression of adhesion molecule CD18 on the surface of polymorphonuclear neutrophil (PMNCD18) 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. (1) When compared with the control group

expression of PMNCD18 and MDA content were enhanced in the ALI 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 signifi cant difference (P<0.01). (2) When compared with the ALI group

the expression of PMN-CD18

MDA content

and W/D ratio were all lower in Tanshinone II A 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). Tan II A 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.