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目的从分子水平探讨博莱霉素诱导肺纤维化小鼠模型的发病机制,为临床诊疗提供新思路。方法从公共基因芯片数据库中下载博莱霉素诱导野生型小鼠肺纤维化的相关基因芯片数据,使用BRB-Array Tools软件对其进行分析,筛选小鼠肺纤维化疾病不同时间点的差异表达基因;并利用DAVID工具进行生物信息学分析。结果 BRB分析发现45 101个差异表达基因,博莱霉素诱导后7 d显著上调1 164个基因(P<0.05,变化倍数>2),下调735个;第14 d上调731个,下调390个(P<0.05,变化倍数>2)。DAVID分析发现上调的基因在细胞周期、p53信号、化学因子信号通路及损伤反应、胶原代谢等生物学过程中有显著富集;而下调的基因在药物代谢信号通路中有显著富集。结论利用生物信息学方法能有效分析基因芯片数据并获取内在信息,为深入认识肺纤维化病程的主要分子事件和细胞信号转导通路改变,并进一步发现肺纤维化的早期诊断标志与治疗靶点提供新的思路。
Objective To investigate the pathogenesis of bleomycin-induced pulmonary fibrosis in mouse model at the molecular level, providing new ideas for clinical diagnosis and treatment. Methods The gene chip data of bleomycin-induced lung fibrosis in wild-type mice was downloaded from the public gene chip database and analyzed by BRB-Array Tools software to screen the differential expression of lung fibrosis in mice at different time points Gene; and using DAVID tools for bioinformatics analysis. Results There were 45 101 differentially expressed genes in BRB assay, 1 164 genes were significantly up-regulated 790 days after bleomycin induction (P <0.05, with a multiple of> 2), down 735, up 731 and 390 down (P <0.05, fold change> 2). DAVID analysis found that upregulated genes in the cell cycle, p53 signaling, chemical signaling pathways and injury response, collagen metabolism and other biological processes were significantly enriched; and down-regulated genes in the drug metabolism signaling pathway significant enrichment. Conclusion Bioinformatics methods can effectively analyze gene chip data and acquire intrinsic information. In order to know more about the major molecular events and cell signal transduction pathways in the course of pulmonary fibrosis, we can further find out the early diagnostic markers and therapeutic targets of pulmonary fibrosis Provide new ideas.