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目的:探讨诱骗受体3(DcR3)对肺纤维化动物模型早期的作用。方法:博莱霉素(BL)气管内灌注复制大鼠肺纤维化模型,ELISA检测支气管肺泡上清中的TGF-β的含量,HE和MASSON染色观察大鼠模型肺组织病理变化。结果:BL+DcR3组TGF-β的含量与对照组比较无统计学差异(P>0.05),与BL组比较有统计学意义(P<0.05)。BL+DcR3组2周的炎症程度和4周的肺纤维化程度明显低于BL组。结论:DcR3早期应用可抑制肺纤维化动物模型TGF-β的产生,从而延缓或阻止肺纤维化的发生。
Objective: To investigate the early role of decoy receptor 3 (DcR3) in animal model of pulmonary fibrosis. Methods: Bleomycin (BL) was intraperitoneally injected into rat pulmonary fibrosis model. The content of TGF-β in bronchoalveolar lavage fluid was detected by ELISA. The pathological changes of lung tissue were observed by HE and MASSON staining. Results: The content of TGF-β in BL + DcR3 group was not significantly different from that in control group (P> 0.05), and there was significant difference between BL + DcR3 group and BL group (P <0.05). The inflammation degree in BL + DcR3 group for 2 weeks and pulmonary fibrosis degree in 4 weeks were significantly lower than those in BL group. Conclusion: Early application of DcR3 can inhibit the production of TGF-β in animal models of pulmonary fibrosis, which can delay or prevent the occurrence of pulmonary fibrosis.