HBV相关肝纤维化患者血浆microRNA的差异表达

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目的探索microRNA在乙型肝炎肝纤维化患者血浆中的差异表达。方法收集2013年至2014年本院收治的经肝组织活检诊断为肝纤维化S2~S3期的患者10例、代偿期肝硬化患者8例,另选取8例健康志愿者作为对照组,采用IlluminaHiSeq测序技术检测各组血浆miRNA表达,对差异表达的miRNA进行聚类分析和靶基因预测;对差异表达miRNA靶基因进行基因本(GO)分析和KEGG通路富集分析。结果与健康对照组相比,肝纤维化组筛选出104个差异miRNA,其中72个表达上调,32个表达下调;肝硬化组筛选出102个miRNA,其中70个表达上调,32个表达下调。两组中均显著上调的共22个,均显著下调的共24个,在上调的miRNA中,共9个miRNA在肝硬化组表达量高于肝纤维化组;下调的miRNA在肝纤维化组与肝硬化组的表达无显著差异。结论肝纤维化患者血浆miRNA表达与健康组有显著差异,这些差异表达的miRNA在肝纤维化进展中起着重要作用,其可能参与肝纤维化发生发展过程中某些信号通路的调控,确切机制尚需进一步深入研究。 Objective To explore the differential expression of microRNA in the plasma of hepatitis B patients with liver fibrosis. Methods Totally 10 patients with liver fibrosis stage S2 ~ S3 diagnosed by liver biopsy in our hospital from 2013 to 2014, 8 patients with decompensated cirrhosis and 8 healthy volunteers were selected as the control group. IlluminaHiSeq sequencing technique was used to detect plasma miRNA expression in each group. Cluster analysis and target gene prediction were performed on the differentially expressed miRNAs. Gene-specific (GO) and KEGG pathway enrichment analyzes of differentially expressed miRNA target genes were performed. Results Compared with healthy controls, 104 differential miRNAs were screened in liver fibrosis group, of which 72 were up-regulated and 32 down-regulated. In the liver cirrhosis group, 102 miRNAs were screened out, of which 70 were up-regulated and 32 were down-regulated. A total of 22 significantly up-regulated in both groups were significantly reduced a total of 24 miRNAs in upregulation, a total of 9 miRNA expression in cirrhosis group was higher than in liver fibrosis group; downregulation of miRNA in liver fibrosis group There was no significant difference with the expression of cirrhosis group. Conclusion The expression of miRNAs in patients with hepatic fibrosis is significantly different from those in healthy subjects. These differentially expressed miRNAs play an important role in the progression of hepatic fibrosis, which may be involved in the regulation of certain signaling pathways during the development of hepatic fibrosis. The exact mechanism Still need further study.
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