title: [STAT1 antisense oligonucleotides inhibit secretion of TNF-alpha, IL-8 and NO in alveolar macrophages of rats suffering from interstitial pulmonary fibrosis].
abstract: OBJECTIVE
  To investigate the effect of signal transducer and activator of transcription 1 (STAT1) antisense oligonucleotides (ASON) on secretion of TNF-alpha, IL-8 and NO by alveolar macrophages (AMs) of rats with bleomycin (BLM)-induced pulmonary fibrosis.
  
  
  METHODS
  Five adult female Wistar rats were intratracheally instilled with BLM. After 7 days, the rats were sacrificed under ketamine anaesthesia and bronchoalveolar lavage (BAL) was performed to obtain AMs. AMs were divided into four groups: STAT1 ASON, STAT1 sense oligonucleotides (SON), dexamethasone (DEX) and control groups. Culture medium was collected at 36 hours after adding STAT1 ASON, STAT1 SON and DEX, respectively. The concentrations of TNF-alpha, IL-8 and NO in the culture medium were detected.
  
  
  RESULTS
  The concentrations of TNF-alpha, IL-8 and NO in STAT1 ASON group were lower than those in STAT1 SON, DEX and control groups (P<0.05). Moreover, the concentrations of TNF-alpha, IL-8 and NO in DEX group were also lower than those in control and STAT1 SON groups (P<0.05). But compared with control group, the concentrations of TNF-alpha, IL-8 and NO in STAT1 SON group was not significantly different (P<0.05).
  
  
  CONCLUSIONS
  STAT1 ASON can inhibit the secretion of TNF-alpha, IL-8 and NO in AMs. STAT1 may become a target for treating pulmonary fibrosis.
authors.affiliation: Department of Respiratory Medicine, Affiliated Hospital of Luzhou Medical College, Luzhou 646000, China. fxm129@163.com
authors.forename: Xian-ming
authors.initials: XM
authors.lastname: Fan
authors.forename: Shi-bo
authors.initials: SB
authors.lastname: Zhang
authors.forename: Chun-tao
authors.initials: CT
authors.lastname: Liu
authors.forename: Bin
authors.initials: B
authors.lastname: Xiong
authors.forename: Zeng-li
authors.initials: ZL
authors.lastname: Wang
mesh_terms: D000818:Animals; D001483:Base Sequence; D001761:Bleomycin / Q000009:adverse effects; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D016209:Interleukin-8 / Q000378:metabolism; D016676:Macrophages, Alveolar / Q000187:drug effects* / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D016376:Oligonucleotides, Antisense / Q000235:genetics / Q000494:pharmacology*; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000473:pathology; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D050794:STAT1 Transcription Factor / Q000235:genetics*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D016209:Interleukin-8; D016376:Oligonucleotides, Antisense; D012333:RNA, Messenger; D050794:STAT1 Transcription Factor; C494081:Stat1 protein, rat; D014409:Tumor Necrosis Factor-alpha; D001761:Bleomycin; D009569:Nitric Oxide