| Objective: To investigate the expression of TGF-β1,CTGF,collagenⅠ,collagenⅢand the role of IFN-γin suppressing bleomycin-induced pulmonary fibrosis in rats.Methods: Seventy-five SD Rats were randomly divided into five groups, ie. a normal group, a bleomycin-induced pulmonary fibrosis model group, a dexamethasone-treated group, a high-dose IFN-γ-treated group (150,000 U/kg) and a low-dose IFN-7-treated group (50,000 U/kg). Five rats in each group were randomly killed in 7th day, 14th day and 28th day after relative treatment respectively, and lung tissue samples were harvested for histopathology study. HE and Masson staining were used to determine the extent of alveolus inflammation and pulmonary fibrosis respectively. Histoimmunochemical method were adapted to determine protein levels of TGF-β1, CTGF, typeⅠcollagen and typeⅢc TGF-β1, CTGF, typeⅠand typeⅢcollagen ollagen in pulmonary tissues.Results: Histopathological study combining HE staining with Masson staining showed that treatment with either dexamethasone or IFN-γ(both high dose and low dose) remarkably meliorated the extent of alveolus inflammation and suppressed pulmonary fibrosis (compared with model group, all P＜0.05). Histoimmunochemical study suggested that both dexamethasone and IFN-γcould inhibit the expression of TGF-β1, CTGF, typeⅠand typeⅢcollagen (compared with model group, all P＜0.05), however, the expression suppression of TGF-β1, typeⅠand typeⅢcollagen is more obvious in high-dose-t-IFN-γ-treated group than those in low-dose-IFN-γ-treated group (p＜0/05).Conclusions: INF-γpossesses apparent anti-fibrosis effect that is similar to dexamethasone but with less side-effect. Such effect may resulted from reduced production of typeⅠand typeⅢcollagen through expression inhibition of cytokines such as TGF-β1 and CTGF.
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