格列卫对肺纤维化小鼠的干预机制

目的 探讨格列卫对小鼠肺纤维化的干预机制.方法 120只C57BL/6小鼠随机分为对照组、模型组、地塞米松组和格列卫组,每组30只.采用气管内注射博莱霉素构建肺纤维化小鼠模型,分别于7、14、21 d随机处死10只动物.免疫组化检测各组肺组织转化生长因子β1(TGF-β1)和α-平滑肌肌动蛋白(α-SMA)的蛋白表达,RT-PCR检测肺组织TGF-β1mRNA含量.结果 模型组各时间点TGF-β1和α-SMA的表达均较对照组显著增加,地塞米松和格列卫处理组各时间点TGF-β1和α-SMA的表达均较模型组显著降低,而地塞米松组和格列卫组的表达水平无显著差异.TGF-β1,与α-SMA表达水平呈直线正相关(r=0.251,P<0.05).结论 格列卫对博莱霉素诱导肺纤维化的抑制作用与其抑制TGF-β1和α-SMA的表达有关.

The Inhibitory Mechanism of Imatinib Mesylate on Bleomycin-Induced Pulmonary Fibrosis in Mice

Objective To explore the inhibitory mechanism of Imatinib mesylate on pulmonary fibrosis induced by bleomycin in mice.Methods A total of 120 C57BL/6 mice were randomly divided into four groups,ie, a control group, a model group, a dexamethasone group, and an Imatinib group.The model of pulmonary fibrosis was established by a single intratracheal instillation of bleomycin in the rats.Then dexamethasone or Imatinib were given intraperitoneally respectively.On day 7,14,21 after the treatment, 10 mice of each group were sacrificed respectively.The expressions of TGF-β1 and α-SMA in lung tissue were analyzed by immunohistochemistry.The mRNA expression of TGF-β1 was measured by RT-PCR.Results The expressions of TGF-β1 and α-SMA in lung tissue at each time point were significantly increased in the model group compared with the control group.And the expressions were obviously decreased in the dexamethasone group and the lmatinib group compared with the model group, with no significant differences between the two treatment groups.The expression of TGF-β1 was positively correlated with the α-SMA expression (r = 0.251, P < 0.05).Conclusion The inhibitory effect of Imatinib on pulmonary fibrosis may be related to the inhibition of TGF-β1 and α-SMA expressions.