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目的研究布洛芬对博莱霉素诱导的肺纤维化的治疗保护作用。方法通过气管内滴注博莱霉素复制小鼠肺纤维化模型,实验分为正常对照组、模型组、布洛芬5 mg/kg治疗组、布洛芬10 mg/kg治疗组和布洛芬20 mg/kg治疗组。采集血清行一氧化氮(NO)化学法检测小鼠血清中NO含量;收集肺泡灌洗液行ELISA方法测定肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)含量;留取肺组织行HE染色观察各组小鼠肺组织形态变化,制备肺组织匀浆测定匀浆中丙二醛(MDA)含量;采用RT-PCR和Western blot检测肺组织中转化生长因子β1(TGF-β1)、Smad2和p-Smad2的表达水平。结果与正常对照组比较,肺纤维化模型组肺组织中发生炎性细胞浸润、肺泡间隔增厚情况,同时血清中NO含量和肺泡灌洗液中炎性因子TNF-α和IL-6含量显著增加,小鼠肺组织中MDA含量也有所增加,TGF-β1和p-Smad2的表达显著升高。经布洛芬治疗后,各项生化指标有所下降,同时肺纤维化损伤得以缓解。结论布洛芬可缓解由博莱霉素诱导的肺纤维化,其作用机制可能与下调NO含量、TNF-α和IL-6等炎性因子含量及调控TGF-β信号通路有关。
Objective To study the protective effect of ibuprofen on bleomycin-induced pulmonary fibrosis. Methods Bleomycin-induced pulmonary fibrosis in mice was induced by intratracheal instillation of bleomycin. The experiment was divided into normal control group, model group, ibuprofen 5 mg / kg treatment group, ibuprofen 10 mg / kg treatment group and ibuprofen 20 mg / kg treatment group. Serum samples were collected for determination of NO in serum by nitric oxide (NO) chemistry method. BALF was collected for the determination of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) The lung tissue was taken out to observe the morphological changes of the lung tissue of the mice in each group by HE staining. The content of malondialdehyde (MDA) in the homogenate of the lung tissue was prepared. The expression of transforming growth factor-β1 (TGF-β1) -β1), Smad2 and p-Smad2 expression levels. Results Compared with the normal control group, inflammatory cell infiltration and thickening of the alveolar septum occurred in the lung tissue of the pulmonary fibrosis model group. Meanwhile, the content of NO in the serum and the levels of inflammatory cytokines TNF-α and IL-6 in the bronchoalveolar lavage fluid were significantly higher Increased, MDA content in mouse lung tissue also increased, the expression of TGF-β1 and p-Smad2 increased significantly. After ibuprofen treatment, the biochemical indicators decreased, while pulmonary fibrosis was alleviated. Conclusion Ibuprofen can relieve bleomycin-induced pulmonary fibrosis and its mechanism may be related to the reduction of NO content, the content of inflammatory cytokines such as TNF-α and IL-6 and the regulation of TGF-β signaling pathway.