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 lun...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 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. Results： （1） When compared with the control group, expression of PMNCD18 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 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）. Conclusion： 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.展开更多
文摘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 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. Results： （1） When compared with the control group, expression of PMNCD18 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 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）. Conclusion： 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.
