Protective Effect of Tanshinone Ⅱ A on Lipopolysaccharide-induced Lung Injury in Rats

Objective:To explore the protective effect of tanshinoneⅡA 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(ALI group),and the tanshinoneⅡA 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 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 signif icant 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 TanshinoneⅡA 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:TanⅡA 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.