title: Tanshinone IIA therapeutically reduces LPS-induced acute lung injury by inhibiting inflammation and apoptosis in mice.
abstract: OBJECTIVE
  To study the effects of tanshinone IIA (TIIA) on lipopolysaccharide (LPS)-induced acute lung injury in mice and the underlying mechanisms.
  
  
  METHODS
  Mice were injected with LPS (10 mg/kg, i.p.), then treated with TIIA (10 mg/kg, i.p.). Seven hours after LPS injection, the lungs were collected for histological study. Protein, LDH, TNF-α and IL-1β levels in bronchoalveolar lavage fluid (BALF) and myeloperoxidase (MPO) activity in lungs were measured. Cell apoptosis and Bcl-2, caspase-3, NF-κB and HIF-1α expression in lungs were assayed.
  
  
  RESULTS
  LPS caused marked histological changes in lungs, accompanied by significantly increased lung W/D ratio, protein content and LDH level in BALF, and Evans blue leakage. LPS markedly increased neutrophil infiltration in lungs and inflammatory cytokines in BALF. Furthermore, LPS induced cell apoptosis in lungs, as evidenced by increased TUNEL-positive cells, decreased Bcl-2 content and increased cleaved caspase-3 content. Moreover, LPS significantly increased the expression of NF-κB and HIF-1α in lungs. Treatment of LPS-injected mice with TIIA significantly alleviated these pathological changes in lungs.
  
  
  CONCLUSIONS
  TIIA alleviates LPS-induced acute lung injury in mice by suppressing inflammatory responses and apoptosis, which is mediated via inhibition of the NF-κB and HIF-1α pathways.
authors.affiliation: Department of Pathology, 88th Hospital of PLA, Taian 271000, China.
authors.forename: Min
authors.initials: M
authors.lastname: Xu
authors.affiliation: Department of Neurology, 88th Hospital of PLA, Taian 271000, China.
authors.forename: Fa-le
authors.initials: FL
authors.lastname: Cao
authors.affiliation: Intensive Care Unit, 88th Hospital of PLA, Taian 271000, China.
authors.forename: Yu-fei
authors.initials: YF
authors.lastname: Zhang
authors.affiliation: Medical Department, 88th Hospital of PLA, Taian 271000, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Shan
authors.affiliation: Department of Pathology, 88th Hospital of PLA, Taian 271000, China.
authors.forename: Xiao-ling
authors.initials: XL
authors.lastname: Jiang
authors.affiliation: Intensive Care Unit, 88th Hospital of PLA, Taian 271000, China.
authors.forename: Xiao-jing
authors.initials: XJ
authors.lastname: An
authors.affiliation: Department of Pathology, 88th Hospital of PLA, Taian 271000, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Xu
authors.affiliation: Department of Pathology, 88th Hospital of PLA, Taian 271000, China.
authors.forename: Xiu-zhi
authors.initials: XZ
authors.lastname: Liu
authors.affiliation: Department of Pathology, 88th Hospital of PLA, Taian 271000, China.
authors.forename: Xiao-yan
authors.initials: XY
authors.lastname: Wang
mesh_terms: D045784:Abietanes / Q000494:pharmacology*; D055371:Acute Lung Injury / Q000139:chemically induced* / Q000188:drug therapy*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D007249:Inflammation / Q000188:drug therapy*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C
chemical_list: D045784:Abietanes; D008070:Lipopolysaccharides; C021751:tanshinone