摘要
目的 :通过研究外源性IL 10对博来霉素诱导大鼠肺纤维化模型的作用 ,探讨IL 10对肺纤维化的作用机理。方法 :5 0只Wistar大鼠随机分为博来霉素组 (A组 )、正常对照组 (D组 )及根据给博来霉素后第 1,15日始按 5μg·kg-1× 3次·(7d) -1给予IL 10腹腔注射分为治疗组 (B组和C组 )。于第 7,14 ,2 8d分批处死动物 ,提取肺组织 ,HE染色行肺纤维化程度分级 ,图象分析仪定量比较肺间隔宽度及免疫组化测定肺组织TNF α、TGF β1、FN蛋白表达。结果 :①B组肺纤维化程度较A组明显减轻 ,TNF α、TGF β1、FN蛋白表达明显下调 (P <0 .0 1) ;②C组肺纤维化程度与A组相似 ,TNF α、TGF β1、FN蛋白表达与A组比较无显著性差异 (P >0 .0 5 )。结论 :IL 10在肺间质纤维化的发生发展中特别是肺泡炎阶段中起重要的抑制作用。
Objective: To investigate the therapeutic mechanism of IL-10 on pulmonary fibrosis through observing the effect of exogenic IL-10 on bleomycin-induced pulmonary fibrosis in rats. Methods: 50 Wistar rats were randomly divided into four groups: the control group(Group D),the bleomycin group(Group A),and two treatment groups(Group B and Group C) which were given IL-10 5 μg·kg -1 ,3 times per week intraperitoneally and at the first (Group B) and the fifteenth day (Group C) the rats were given bleomycin respectively. All rats were killed at day 7,14,28 after bleomycin treatment respectively. The thickness of alveolar wall, the area of mesenchyma in lung tissue were measured by HE staining. Immunohistochemical evaluation was used to detect the expression of TNF-α,TGF-β and FN protein. Results: The degrees of fibrosis,the levels of the expression of TNF-α,TGF-β and FN protein were decreased significantly in Group B as compared with those in Group A(P<0.01) but not significantly in the Group C(P>0.05). Conclusion: IL-10 seems plays an important inhibition role in the development of the pulmonary fibrosis, especially in the alveolitis phase.
出处
《武汉大学学报(医学版)》
CAS
2004年第2期159-161,165,F003,共5页
Medical Journal of Wuhan University