title: Different effects of farrerol on an OVA-induced allergic asthma and LPS-induced acute lung injury.
abstract: BACKGROUND
  Farrerol, isolated from rhododendron, has been shown to have the anti-bacterial activity, but no details on the anti-inflammatory activity. We further evaluated the effects of this compound in two experimental models of lung diseases.
  
  
  RESULTS
  For the asthma model, female BALB/c mice were challenged with ovalbumin (OVA), and then treated daily with farrerol (20 and 40 mg/kg, i.p.) as a therapeutic treatment from day 22 to day 26 post immunization. To induce acute lung injury, female BALB/c mice were injected intranasally with LPS and treated with farrerol (20 and 40 mg/kg, i.p.) 1 h prior to LPS stimulation. Inflammation in the two different models was determined using ELISA, histology, real-time PCR and western blot. Farrerol significantly regulated the phenotype challenged by OVA, like cell number, Th1 and Th2 cytokines levels in the BALF, the OVA-specific IgE level in the serum, goblet cell hyperplasia in the airway, airway hyperresponsiveness to inhaled methacholine and mRNA expression of chemokines and their receptors. Furthermore, farrerol markedly attenuated the activation of phosphorylation of Akt and nuclear factor-κB (NF-κB) subunit p65 both in vivo and in vitro. However, farrerol has no effect on the acute lung injury model.
  
  
  CONCLUSIONS
  Our finding demonstrates that the distinct anti-inflammatory effect of farrerol in the treatment of asthma acts by inhibiting the PI3K and NF-κB pathway.
authors.affiliation: Institute of Zoonoses, College of Animal Science and Veterinary Medicine, Jilin University, Changchun, Jilin, People's Republic of China.
authors.forename: Xinxin
authors.initials: X
authors.lastname: Ci
authors.forename: Xiao
authors.initials: X
authors.lastname: Chu
authors.forename: Miaomiao
authors.initials: M
authors.lastname: Wei
authors.forename: Xiaofeng
authors.initials: X
authors.lastname: Yang
authors.forename: Qinren
authors.initials: Q
authors.lastname: Cai
authors.forename: Xuming
authors.initials: X
authors.lastname: Deng
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D002867:Chromones / Q000627:therapeutic use*; D016207:Cytokines / Q000097:blood; D005260:Female; D007073:Immunoglobulin E / Q000097:blood; D008070:Lipopolysaccharides / Q000276:immunology / Q000633:toxicity; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000378:metabolism; D010047:Ovalbumin / Q000276:immunology; D010641:Phenotype; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D019707:Receptors, Chemokine / Q000378:metabolism; D015398:Signal Transduction; D018417:Th1 Cells / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D018925:Chemokines; D002867:Chromones; D016207:Cytokines; D008070:Lipopolysaccharides; D016328:NF-kappa B; D019707:Receptors, Chemokine; C015881:farrerol; D007073:Immunoglobulin E; D010047:Ovalbumin; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt