[An experimental study on the effect of azithromycin treatment in bleomycin-induced pulmonary fibrosis of rats].
OBJECTIVE
To evaluate the therapeutic effects and mechanism of azithromycin treatment in bleomycin-induced pulmonary fibrosis of rats.


METHODS
Animal model of bleomycin-A5-induced pulmonary fibrosis was established in rats.36 animal models were divided into two groups: a bleomycin-induced pulmonary fibrosis group and a azithromycin group in which the animal models were treated with azithromycin (80 mg/kg once a day for three continuous days in a week). The animals of the two groups were killed at the first,second and fourth week respectively. Another six rats constituted a normal control group, instillated withsaline intratracheally and killed at the first week. Pathological changes activity of nuclear factor kappaB (NF-kappaB) of alveolar macrophage, cytokine tumor necrosis factor (TNF) alpha, transforming growth factor-beta (TGF-beta) mRNA expression and protein levels of alveolar macrophage and lung tissue were studied or measured.


RESULTS
Amelioration of alveolitis and lung fibrosis after treatment with azithromycin was shown in pathological section (P < 0.05). The activity of NF-kappaB was significantly higher in one-week pulmonary fibrosis model than that in normal control and its level in alveolar macrophage reduced (67.2%) after treatment with azithromycin. The level of protein and mRNA of TNFalpha, TGF-beta in lung tissue and alveolar macrophage was increased in the early stage of pulmonary fibrosis and reduced after treatment with azithromycin (P < 0.05).


CONCLUSIONS
It is suggested that azithromycin might be a therapeutic drug for pulmonary fibrosis in the future. Azithromycin reduced the degree of alveolitis and fibrosis through inhibition of the activity of NF-kappaB and the expression of TNFalpha, TGF-beta mRNA and lowering the level of protein in alveolar macrophage and lung tissue in the early stage of pulmonary fibrosis. This might be one of the mechanisms of azithromycin treatment in pulmonary fibrosis.
Chen
J
J
Department of Pulmonary Medicine, The First Hospital, Beijing Medical University, Beijing 100034.
He
B
B
Li
Y
Y
Wang
G
G
Zhang
W
W
D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D001761:Bleomycin; D004917:Erythromycin / Q000627:therapeutic use*; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D016212:Transforming Growth Factor beta / Q000096:biosynthesis / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics
D000900:Anti-Bacterial Agents; D016328:NF-kappa B; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D001761:Bleomycin; D004917:Erythromycin