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Protective effect of tanshinone II A on lipopolysaccharide-induced lung injury in rats
  
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KeyWord:CD18 adhesion molecule  acute lung injury  tanshinone II A  malondialdehyde  coagulation abnormality
Author NameAffiliationE-mail
Dr. Xue-mei Shi Department of Respiratory Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China sxmxi2002@163.com 
Liang Huang Department of Emergency, First Affiliated Hospital to Jiangxi Medical College, China  
Sheng-dao Xiong Department of Respiratory Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China  
Xian-yang Zhong Department of Nephrology, The 421 Hospital of PLA, Guangzhou, China  
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Abstract:
      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 (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. Results (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). 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.
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