title: [The effect of erythromycin on NF-kappa B activation and cytokines mRNA expression in bleomycin-induced pulmonary fibrosis in rats].
abstract: OBJECTIVE
  To evaluate the effect of erythromycin (EM) on nuclear factor-kappa B (NF-kappa B) activation and cytokines mRNA expression in bleomycin-induced pulmonary fibrosis in rats.
  
  
  METHODS
  Wistar rats were divided into three groups of 27 as follow: BLM-group received intratracheal instillation of single dose BLM 5 mg/kg. EM treated-group received intratracheal instillation of BLM 5 mg/kg and an oral instillation EM 100 mg.kg-1.d-1. Control group received intratracheal and oral instillation of normal saline. Animals of all three groups were sacrificed on the 4th, 7th and the 28th day separately. NF-kappa B activation in alveolar macrophages (AM) was investigated by electrophoretic mobility shift assay. The expressions of IL-1 beta and TGF-beta mRNA in lung were evaluated by Northern blot analysis. The pathological changes of lung tissue were analyzed quantitatively by computer gray scan.
  
  
  RESULTS
  On the 4th and 7th day, the activities of NF-kappa B in AM were significantly increased in BLM-group compared with those of control group (P < 0.05), while they were significantly decreased in EM treated-group compared with BLM-group (P < 0.05). On the 7th day, the expressions of IL-1 beta and TGF-beta mRNA in lung were significantly decreased in EM treated-group compared with those in BLM-group. Pathologically, EM decreased exudation of inflammatory cells in the early response as well as degree of fibrosis in the late stage in the BLM-induced pulmonary fibrosis.
  
  
  CONCLUSIONS
  These results indicate that NF-kappa B is involved in the inflammatory response in BLM-induced pulmonary fibrosis in rats, EM has inhibitory effect on NF-kappa B activation, IL-1 beta and TGF-beta mRNA expression, by which it ameliorated acute lung injury and fibrosis those tested rats.
authors.affiliation: Department of Respiratory Medicine, First Hospital, Beijing Medical University, Beijing 100034.
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.forename: B
authors.initials: B
authors.lastname: He
authors.forename: H
authors.initials: H
authors.lastname: Wang
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001761:Bleomycin; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D004195:Disease Models, Animal; D004917:Erythromycin / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects*; D007375:Interleukin-1 / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D016328:NF-kappa B / Q000096:biosynthesis* / Q000235:genetics; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D016212:Transforming Growth Factor beta / Q000096:biosynthesis / Q000235:genetics
chemical_list: D000900:Anti-Bacterial Agents; D016207:Cytokines; D007375:Interleukin-1; D016328:NF-kappa B; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D001761:Bleomycin; D004917:Erythromycin