title: Triptolide suppresses airway goblet cell hyperplasia and Muc5ac expression via NF-κB in a murine model of asthma.
abstract: BACKGROUND
  We have reported that triptolide inhibited pulmonary inflammation in patients with steroid-resistant asthma. In the present study, we investigated whether suppresses airway remodeling and goblet cell hyperplasia, studied the mechanism of triptolide on mucin5ac (Muc5ac) expression in a murine model of asthma.
  
  
  METHODS
  BALB/c mice were sensitized to intraperitoneal ovalbumin (OVA) followed by repetitive ovalbumin challenge for 6 weeks. Treatments included triptolide (40 μg/kg) and dexamethasone (2mg/kg). The area of bronchial airway (WAt/Pbm), smooth muscle (WAm/Pbm) and mucus index were assessed 24h after the final OVA challenge. Levels of Muc5ac were assessed by ELISA, immunohistology and real-time PCR. Western blot was performed to analyze the phosphorylation of NF-κB p65.
  
  
  RESULTS
  Triptolide and dexamethasone significantly reduced allergen-induced increases in the thickness of bronchial airway, smooth muscle and goblet cell hyperplasia. Levels of lung Muc5ac and Muc5ac mRNA were significantly reduced in mice treated with triptolide and dexamethasone. Phosphorylation of NF-κB p65 was significantly reduced in mice treated with triptolide and dexamethasone.
  
  
  CONCLUSIONS
  Triptolide may inhibit airway goblet cell hyperplasia and Muc5ac expression in asthmatic mice via NF-κB. It may be a potential drug for the treatment of patients with severe asthma.
authors.affiliation: Department of Respiratory Medicine, Sun Yat-Sen Memorial Hospital, Institute for Respiratory Disease of Sun Yat-sen University, Sun Yat-sen University, Guangzhou, Guangdong Province 510120, China.
authors.forename: Ming
authors.initials: M
authors.lastname: Chen
authors.affiliation: Department of Respiratory Medicine, Sun Yat-Sen Memorial Hospital, Institute for Respiratory Disease of Sun Yat-sen University, Sun Yat-sen University, Guangzhou, Guangdong Province 510120, China.
authors.forename: Zhiqiang
authors.initials: Z
authors.lastname: Lv
authors.affiliation: Department of Geratology, The Second People's Hospital of Shenzhen, Shenzhen 518000, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.affiliation: Department of Respiratory Medicine, Sun Yat-Sen Memorial Hospital, Institute for Respiratory Disease of Sun Yat-sen University, Sun Yat-sen University, Guangzhou, Guangdong Province 510120, China.
authors.forename: Linjie
authors.initials: L
authors.lastname: Huang
authors.affiliation: Department of Respiratory Medicine, Sun Yat-Sen Memorial Hospital, Institute for Respiratory Disease of Sun Yat-sen University, Sun Yat-sen University, Guangzhou, Guangdong Province 510120, China.
authors.forename: Xiaoling
authors.initials: X
authors.lastname: Lin
authors.affiliation: Department of Respiratory Medicine, Sun Yat-Sen Memorial Hospital, Institute for Respiratory Disease of Sun Yat-sen University, Sun Yat-sen University, Guangzhou, Guangdong Province 510120, China.
authors.forename: Jianting
authors.initials: J
authors.lastname: Shi
authors.affiliation: Department of Respiratory Medicine, Sun Yat-Sen Memorial Hospital, Institute for Respiratory Disease of Sun Yat-sen University, Sun Yat-sen University, Guangzhou, Guangdong Province 510120, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.affiliation: Department of Respiratory Medicine, Sun Yat-Sen Memorial Hospital, Institute for Respiratory Disease of Sun Yat-sen University, Sun Yat-sen University, Guangzhou, Guangdong Province 510120, China.
authors.forename: Ruiyun
authors.initials: R
authors.lastname: Liang
authors.affiliation: Department of Respiratory Medicine, Sun Yat-Sen Memorial Hospital, Institute for Respiratory Disease of Sun Yat-sen University, Sun Yat-sen University, Guangzhou, Guangdong Province 510120, China. Electronic address: shanpingjiang@126.com.
authors.forename: Shanping
authors.initials: S
authors.lastname: Jiang
mesh_terms: D056151:Airway Remodeling; D000818:Animals; D001249:Asthma / Q000188:drug therapy* / Q000473:pathology* / Q000503:physiopathology; D015153:Blotting, Western; D001980:Bronchi / Q000473:pathology*; D001992:Bronchoalveolar Lavage Fluid; D004195:Disease Models, Animal; D004224:Diterpenes / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D004852:Epoxy Compounds / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D020397:Goblet Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D006965:Hyperplasia; D006984:Hypertrophy; D008807:Mice, Inbred BALB C; D055271:Mucin 5AC / Q000235:genetics / Q000378:metabolism*; D009093:Mucus / Q000187:drug effects; D016328:NF-kappa B / Q000378:metabolism*; D010616:Phenanthrenes / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D010766:Phosphorylation / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D004224:Diterpenes; D004852:Epoxy Compounds; C524679:Muc5ac protein, mouse; D055271:Mucin 5AC; D016328:NF-kappa B; D010616:Phenanthrenes; D012333:RNA, Messenger; D051996:Transcription Factor RelA; C001899:triptolide
keywords: Asthma; Goblet cell hyperplasia; Muc5ac; NF-κB; Triptolide