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机构地区:[1]军事医学科学院卫生装备研究所,天津300161 [2]武警医学院天津市职业与环境危害生物标志物重点实验室,天津300162
出 处:《军事医学科学院院刊》2008年第3期271-275,共5页Bulletin of the Academy of Military Medical Sciences
基 金:天津市自然基金面上项目(06YFJMJC09800)
摘 要:目的:探讨肺纤维化过程中细胞因子的调控网络。方法:应用荟萃分析筛选Wistar大鼠肺纤维化过程中肺组织的相关细胞因子。通过三次样条插值,采用线性微分方程模型进行网络调控的研究。结果:参与肺纤维化形成的相关细胞因子为IFN-γ,IL-10,IL-13,IL-18,IL-4,IL-5,IL-6,IL-8,IGF-1,MCP-1,PDGF,TGF-β1,TNF-α,MMP-2,MMP-9,EGF。构建的调控通路中重要的细胞因子节点为IFN-γ,IL-10,IL-13,IL-18,IL-6,IGF-1,PDGF,TGF-β1,TNF-α。结论:肺纤维化细胞因子网络由关键的细胞因子组成,非关键节点的细胞因子可能因致纤维化作用较小或仅参与炎症作用而未参加网络的调控。Objective:To explore cytokine network of pulmonary fibrosis. Methods: The cytokines of pulmonary tissue in lung fibrosis were screened by meta analysis. Then the potential regulatory pathway of cytokines was analyzed with a cubic spline interpolation and a linear differential model. Results: The related cytokines participating in pulmonary fibrosis were IFN-γ, IL-10, IL-13, IL-18, IL-4, IL-5,IL-6,IL-8,IGF-1, MCP-1, PDGF, TGF-β1 ,TNF-α,MMP-2, MMP-9, and EGF by meta analysis. The key eytokine nodes of the regulating pathway were IFN-γ,IL-10, IL-13, IL-18, IL-6, IGF-1, PDGF, TGF-β1 ,and TNF-α. Conclusion: The cytokinenetwork of pulmonary fibrosis was composed of the key cytokines, but non-key cytokines were not in the networks due to a minor role in inducing pulmonary fibrosis or merely participating in inflammation.
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