Effect Of Interleukin-10 On Pulmonary Fibrosis Induced By Bleomycin In Rats

Backgroud and Objective The pathogenesis of pulmonary fibrosis is complicated,it is characterized with myofibroblast hyperplasia and deposition of collage protein.Studying demonstrated that the pathogenesis is associated with disorders of all kinds of cytokines or growth factors. Interleukin-10 (IL-10),as a powerful cytokine regulatory factor ,whose role in pulmonary fibrosis is not yet clear. This experiment is to investigate the effect of IL-10 on bleomycin-induced pulmonary fibrosis in rats by administrating exogenic IL-10 at its different stages .Materials and Methods In this study, 50 wistar rats were randomly divided into four groups:The model group(GroupA),the control group(GroupD), and two treatement groups (GroupB and GroupC). On experimental day(dayO) , the rats were intratracheally instilled with bleomycin(5mg/kg body weight)or sterile saline. Two treatement groups were given IL-10 5 g kg-1,3 times per week intraperitoneally from the first day(GroupB) or from the fifteenth day (GroupC) respectively. On day 7, 14, 28 after instillation,5 rats of group (A, B, D)were sacrificed, and all rats of group (C) were sacrificed On day 28. The lungs were harvested for histopathological examination. The thickness of alveolar wall, the areas of mesenchyma in lung tissue were measured by HE staining. Immunohistochemical evaluation was to detect the expression of TNF-α , TGF-β1, FN protein.Results (1) The degrees of alveolitis and pulmonary fibrosis of the model group was increased remarkably on day 7,14,28 compared with the control group (P<0.05), The expression of TNF- α , TGF- β1, FN protein of model group on day 7, 14, 28 was remarkably increased compared with the control group (P<0.05); (2)The degrees of fibrosis and the expression of TNF-α, TGF- β1 , FN protein are decreased significantly in Group B compared with Group A( P<0.05) but not significantly in Group C.Conclusion IL-10 seems plays an important inhibition role in the development of the pulmonary fibrosis, especially in the alveolitis phase.