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目的研究从microRNAs角度揭示轻度慢性乙型肝炎炎症活动的分子机制。方法将符合标准的病例分为轻度慢性乙型肝炎组与慢性HBV携带者组,借助Agilent Human microRNA 8×60k微阵列芯片检测血浆中microRNAs表达谱,求得两组间的差异表达microRNAs谱(P<0.05),借助microRNAs生物信息学分析软件预测其靶基因并对靶基因进行GO功能富集分析和pathway分析。结果两组间的差异表达microRNAs共65条(P<0.05),38条上调,27条下调;GO分析及pathway分析得到其功能主要涉及细胞增殖、生物黏附、生物合成过程的正/负调控、大分子生物合成过程中的正/负调控、蛋白氨基酸的磷酸化、RNA的生物合成过程、Wnt信号通路、MAPK信号通路、Notch信号传导途径、Hedgehog信号通路、T细胞受体信号通路、TGF-β信号通路、mTOR信号通路、趋化因子信号通路JAK-STAT信号通路、钙离子信号通路等。结论轻度慢性乙型肝炎炎症活动受特异性microRNAs调控,其涉及多个生命过程及通路。
Objective To study the molecular mechanism of inflammatory activity in mild chronic hepatitis B from the perspective of microRNAs. Methods According to the criteria, the patients were divided into two groups: mild chronic hepatitis B group and chronic HBV carriers group. MicroRNAs expression profiles were detected by Agilent Human microRNA 8 × 60k microarray. Differentially expressed microRNAs profiles P <0.05). The microarray bioinformatics software was used to predict the target genes and GO gene enrichment and pathway analysis of the target genes were performed. Results A total of 65 microRNAs (P <0.05) were differentially expressed between the two groups, 38 up-regulated and 27 down-regulated. The positive and negative regulation of cell proliferation, bioadhesion and biosynthesis were found by GO analysis and pathway analysis. Positive / negative regulation of macromolecular biosynthesis, protein amino acid phosphorylation, RNA biosynthesis, Wnt signaling pathway, MAPK signaling pathway, Notch signaling pathway, Hedgehog signaling pathway, T cell receptor signaling pathway, TGF- β signaling pathway, mTOR signaling pathway, chemokine signaling pathway JAK-STAT signaling pathway, calcium signaling pathway. Conclusion The inflammatory activity of mild chronic hepatitis B is regulated by specific microRNAs, which involves multiple life processes and pathways.