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目的 研究大鼠肺纤维化中单核细胞趋化蛋白- 1 (MCP -1) 和转化生长因子- β(TGF- β) 的表达及己酮可可碱对它们的影响。方法 采用气管内灌注博来霉素的方法建立大鼠肺纤维化模型, 设对照组、模型组和己酮可可碱治疗组, 每组12只, 再各分为第7天和第28天组。测定28 d时肺组织中羟脯氨酸含量和溶胶原活性以判断纤维化程度及治疗效果, 同时用免疫组化法观察7、28 d时MCP 1和TGF -β在肺组织中的表达变化。结果 模型组羟脯氨酸含量显著增高、溶胶原活性下降, 而己酮可可碱治疗组与对照组比较无明显差异。与对照组比较, 模型组MCP- 1 和TGF- β的表达显著增高(均P<0. 01), 己酮可可碱治疗组也有所增高, 但均明显低于模型组(均P<0. 01)。结论 己酮可可碱可抑制鼠肺纤维化, 调节MCP- 1和TGF- β的表达可能是己酮可可碱抑制鼠肺纤维化的机制之一。
Objective To investigate the expression of monocyte chemoattractant protein - 1 (MCP - 1) and transforming growth factor - β (TGF - β) in rat pulmonary fibrosis and the effects of pentoxifylline on them. Methods Pulmonary fibrosis model was established by intratracheal infusion of bleomycin. The rats in the control group, model group and pentoxifylline-treated group were divided into 7 groups and 12 groups. The content of hydroxyproline and the activity of collagen in the lung tissue were measured at 28 days to determine the degree of fibrosis and the therapeutic effect. The expression of MCP 1 and TGF-β in lung tissues at 7 and 28 days were observed by immunohistochemistry . Results The content of hydroxyproline in model group was significantly increased and the activity of sol was decreased. There was no significant difference between pentoxifylline treatment group and control group. Compared with the control group, the expression of MCP-1 and TGF-β in the model group were significantly increased (all P <0.01), pentoxifylline treatment group also increased, but were significantly lower than the model group (P <0. 01). CONCLUSION Pentoxifylline can inhibit rat pulmonary fibrosis. Regulating the expression of MCP-1 and TGF-β may be one of the mechanisms by which pentoxifylline may inhibit rat pulmonary fibrosis.