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目的:通过基因芯片技术研究大鼠肺纤维化不同时间点和应用黄芪甲甙干预后的基因差异表达,寻找肺纤维化的致病基因和应用黄芪甲甙进行干预治疗相关的靶基因。方法:用含41000个基因的安捷伦大鼠芯片同模型组7天和模型组28天以及BLM+黄芪甲甙组28天的大鼠肺组织进行杂交,利用安捷伦基因扫描仪扫描杂交图像,模型组7天和BLM+黄芪甲甙组与模型组28天进行比较,筛选Ratio值大于2的差异基因进行分析,重复3次。结果:模型组28天对比7天共有2063个基因表达差异,筛选109个基因,43个上调,66个下调。黄芪甲甙28天组对比模型28天组4269个基因表达差异,筛选68个基因,45个上调,23个下调。通过GO和PATHWAY分析软件,提示有不同的功能分类和信号传导途径。结论:基因芯片为了解肺纤维化不同时间点的基因表达的异常,以及黄芪甲甙治疗肺纤维化的可能机制和药物靶基因的提供了理论基础。
OBJECTIVE: To study the differentially expressed genes of lung fibrosis and astragaloside at different time points by gene chip technology in order to find the pathogenic genes of pulmonary fibrosis and the target genes related to the intervention of astragaloside. METHODS: The lungs of rats with 41000 genes were stained with Agilent microarray for 7 days and model group for 28 days and BLM + Astragaloside group for 28 days. The hybridization images were obtained by Agilent gene scanner. The model group 7 Day and BLM + Astragaloside group and model group compared for 28 days, the screening ratio of more than 2 genes were analyzed, repeated 3 times. Results: In the model group, there were 2063 gene expression differences between 28 days and 7 days, 109 genes were screened, 43 were up-regulated and 66 were down-regulated. Astragaloside 28 days group comparison model 2869 day group 4269 gene expression differences, screening 68 genes, 45 were up-regulated, 23 down. Through GO and PATHWAY analysis software, suggesting different functional classifications and signaling pathways. Conclusion: Gene chip provides a theoretical basis for understanding the gene expression abnormality at different time points of pulmonary fibrosis and the possible mechanism of astragaloside treatment of pulmonary fibrosis and drug target gene.