title: Acute lung injury induced by lipopolysaccharide is inhibited by wogonin in mice via reduction of Akt phosphorylation and RhoA activation.
abstract: OBJECTIVE
  Neutrophil infiltration into the lung is the critical characteristic of acute lung injury (ALI), which is a clinical state with acute inflammatory syndrome. Up to now, there is no effective medicine for ALI. Wogonin has been shown to posses serval biological activities including anti-inflammation, anti-oxidant and anti-carcinoma.
  
  
  METHODS
  Acute lung injury was induced by intratracheal injection of LPS, and wogonin at various concentrations was injected intraperitoneally 30 min prior to LPS. Contents of myeloperoxidase (MPO) and expression of chemokines and adhesion molecules were determined by commercially and ELISA assay kits, respectively. Akt phosphorylation and RhoA activation were measured by western blot and RhoA pull-down activation assay, respectively.
  
  
  RESULTS
  Neutrophil infiltration was reduced by wogonin in a concentration-dependent manner in the LPS-induced ALI mice model. LPS-induced proinflammatory cytokines and adhesion molecules were inhibited by wogonin in bronchoalveolar lavage fluid (BALF) with LPS-induced ALI. Furthermore, wogonin suppressed Akt phosphorylation and RhoA activation in lungs in LPS-induced ALI. The similar parallel trend was observed as wogonin reduced LPS-induced neutrophils infiltration, proinflammatory cytokines generation, adhesion molecules expression, Akt phosphorylation, and RhoA activation.
  
  
  CONCLUSIONS
  These results suggested that the effects of wogonin in LPS-induced ALI were induced by inhibition of Akt phosphorylation and RhoA activation.
authors.affiliation: Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan.
authors.forename: Yen-Cheng
authors.initials: YC
authors.lastname: Yeh
authors.affiliation: Department of Biotechology and Laboratory Science in Medicine, Yang-Ming University, Taipei, Taiwan.
authors.forename: Ching-Ping
authors.initials: CP
authors.lastname: Yang
authors.affiliation: School of Public Health, Chung Shan Medical University, Taichung, Taiwan.
authors.forename: Shiuan-Shinn
authors.initials: SS
authors.lastname: Lee
authors.affiliation: Medical Education Center, Kaohsiung Armed Forces General Hospitl, Kaohsiung City, Taiwan.|Institute of Biochemistry and Biotechnology, Chung Shang Medical University, Taichung, Taiwan.
authors.forename: Chi-Ting
authors.initials: CT
authors.lastname: Horng
authors.affiliation: School of Pharmacy, China Medical University, Taichung, Taiwan.
authors.forename: Hung-Yi
authors.initials: HY
authors.lastname: Chen
authors.affiliation: Department of Optometry, Shu Zen Junior College of Medicine and Management, Kaohsiung, Taiwan.
authors.forename: Ta-Hsiung
authors.initials: TH
authors.lastname: Cho
authors.affiliation: Department of Anatomy, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
authors.forename: Ming-Ling
authors.initials: ML
authors.lastname: Yang
authors.affiliation: Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.|Department of Pharmacy, Chung Shan Medical University Hospital, Taichung, Taiwan.
authors.forename: Chien-Ying
authors.initials: CY
authors.lastname: Lee
authors.affiliation: Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
authors.forename: Miao-Cing
authors.initials: MC
authors.lastname: Li
authors.affiliation: Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.|Department of Pharmacy, Chung Shan Medical University Hospital, Taichung, Taiwan.
authors.forename: Yu-Hsiang
authors.initials: YH
authors.lastname: Kuan
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism / Q000517:prevention & control*; D000818:Animals; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage / Q000627:therapeutic use*; D044950:Flavanones / Q000008:administration & dosage / Q000627:therapeutic use*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D008813:Mice, Inbred ICR; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D031363:Scutellaria / Q000737:chemistry; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D020741:rho GTP-Binding Proteins / Q000378:metabolism*; D020742:rhoA GTP-Binding Protein
chemical_list: D004365:Drugs, Chinese Herbal; D044950:Flavanones; D008070:Lipopolysaccharides; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D051057:Proto-Oncogene Proteins c-akt; C526380:RhoA protein, mouse; D020741:rho GTP-Binding Proteins; D020742:rhoA GTP-Binding Protein; C085514:wogonin
keywords: Akt; RhoA; acute lung injury; adhesion molecules; cytokines; wogonin