title: [Protective effect of tanshinol on the hepatopulmonary syndrome in rat].
abstract: OBJECTIVE
  To explore the mechanism of tanshinol on alleviate the inflammatory injury of lung tissue in rat hepatopulmonary syndrome (HPS).
  
  
  METHODS
  SD rats were randomly divided into normal control group (n = 8), hepatopulmonary syndrome (HPS) group (n = 11) and tanshinol intervention group (n = 9). HE staining was used to observe the histopathology changes of pulmonary and hepatic tissues, and to count the number of macrophages in lung tissues. The activity of alanine transferase (ALT) and concentrations of endotoxin, tumor necrosis factor-a (TNF-alpha) and homocystein (Hcy) in plasma were detected. The concentrations of TNF-alpha, nitric oxide (NO) and malondialdehyde (MDA) and the activity of inducible nitric oxide synthase (iNOS) in the lung tissues were measured, respectively.
  
  
  RESULTS
  Thickened alveolar septum and increased macrophages were observed in lungs in HPS rat. After administered with tanshinol, the pulmonary pathological changes were alleviated and the number of macrophages in lung tissue was decreased compared with HPS group. The activity of ALT and the concentrations of endotoxin, TNF-alpha and Hcy in plasma ,and TNF-alpha, iNOS, NO and MDA in lung tissue in HPS group were higher than those of normal control group; meanwhile, those tanshinol group were less those that of HPS group.
  
  
  CONCLUSIONS
  Tanshinol may play an important role in delaying the development of HPS through protecting liver or directly antagonizing the effect of intestinal endotoxemia so as to alleviate the inflammatory reaction in lung tissue.
authors.forename: Jian-Tao
authors.initials: JT
authors.lastname: Jia
authors.forename: Hui-Ying
authors.initials: HY
authors.lastname: Zhang
authors.forename: Li-Na
authors.initials: LN
authors.lastname: Lai
authors.forename: Xu-Jiong
authors.initials: XJ
authors.lastname: Li
authors.forename: Xiao-Xia
authors.initials: XX
authors.lastname: Tian
authors.forename: Li-Li
authors.initials: LL
authors.lastname: Zhang
authors.forename: Min-Li
authors.initials: ML
authors.lastname: Lv
authors.forename: Zhong-Fu
authors.initials: ZF
authors.lastname: Zhao
authors.forename: De-Wu
authors.initials: DW
authors.lastname: Han
authors.forename: Ji
authors.initials: J
authors.lastname: Cheng
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D002109:Caffeic Acids / Q000494:pharmacology*; D004195:Disease Models, Animal; D004731:Endotoxins / Q000097:blood; D020065:Hepatopulmonary Syndrome / Q000188:drug therapy* / Q000473:pathology; D006710:Homocysteine / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008264:Macrophages / Q000187:drug effects / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D002109:Caffeic Acids; D004731:Endotoxins; D014409:Tumor Necrosis Factor-alpha; C585969:tanshinol; D006710:Homocysteine; D009569:Nitric Oxide; D008315:Malondialdehyde; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D000410:Alanine Transaminase