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目的 :探讨糖皮质激素对肺间质纤维化的治疗效果及其作用机制。方法 :18只ICR小白鼠在气管内注入博莱霉素后 ,随机分为 2组 :博莱霉素组 (10只 )和氢化可的松组 (8只 )。另取 8只小白鼠气管内注入 5 0 μl生理盐水作为对照。 30天后抽取血液 ,ELISA法测定血清肿瘤坏死因子 α(TNF α)含量 ,并分离肺组织 ,作病理组织学检查 ;用S P免疫组化法测定转化生长因子 β1(TGF β1)表达。结果 :氢化可的松组肺间质纤维化及其TGF β1表达程度较博莱霉素组显著减轻 (P <0 .0 0 5 ) ;纤维化区TGF β1表达程度与肺纤维化 (r=0 .6 6 9,P <0 .0 1)和间质炎症程度明显相关 (r=0 .5 6 3,P <0 .0 5 )。但两组血清TNF α含量差异无显著性。结论 :糖皮质激素能抑制博莱霉素所致的肺间质纤维化和炎症 ,作用机制可能与TGF β1表达受抑制有关。
Objective: To investigate the therapeutic effect of glucocorticoids on pulmonary interstitial fibrosis and its mechanism. Methods: Eighteen ICR mice were randomly divided into two groups: bleomycin group (n = 10) and hydrocortisone group (n = 8) after intratracheal injection of bleomycin. Another 8 mice tracheal intratracheal injection of 50 μl of saline as a control. Thirty days later, blood samples were taken for determination of serum tumor necrosis factor α (TNFα) by ELISA. The lung tissues were separated for histopathological examination. The expression of transforming growth factor β1 (TGFβ1) was detected by SP immunohistochemistry. Results: Compared with bleomycin group, the expression of TGF-β1 in lung tissue of hydrocortisone group was significantly decreased (P <0.05); the expression of TGF-β1 in fibrosis area was significantly correlated with pulmonary fibrosis (r = 0 6 6 9, P 0 01) and interstitial inflammation were significantly correlated (r = 0.563, P <0.05). However, there was no significant difference between the two groups in serum TNFα. Conclusion: Glucocorticoids can inhibit bleomycin induced interstitial lung fibrosis and inflammation, the mechanism may be related to inhibition of TGF β1 expression.