目的:基于高通量测序技术探讨益糖康对糖尿病小鼠外周血miRNA表达谱的影响。方法:从15只C57BL/6小鼠中随机选取5只作为空白组,其余小鼠采用高脂饲料结合腹腔注射链脲佐菌素(100 mg·kg^(-1))的方式建立糖尿病模型。将造模成功的小...目的:基于高通量测序技术探讨益糖康对糖尿病小鼠外周血miRNA表达谱的影响。方法:从15只C57BL/6小鼠中随机选取5只作为空白组,其余小鼠采用高脂饲料结合腹腔注射链脲佐菌素(100 mg·kg^(-1))的方式建立糖尿病模型。将造模成功的小鼠随机分为模型组和益糖康组(32.2 g·kg^(-1)),每组5只,灌胃9周,每日1次,每周检测空腹血糖(fasting blood glucose,FBG)。采用高通量测序技术检测小鼠外周血miRNA表达情况,筛选差异表达miRNA,并通过miRanda数据库预测靶基因。最后,针对靶基因进行基因本体(Gene Ontology,GO)和京都基因与基因组百科全书(Kyoto Encylopaedia of Genes and Genomes,KEGG)富集分析。结果:给药第1—9周,与空白组比较,模型组小鼠FBG升高(P<0.01);给药第4—9周,与模型组比较,益糖康组小鼠FBG降低(P<0.05,P<0.01)。与模型组比较,益糖康组小鼠外周血8个miRNA表达上调,包括miR-434-3p、miR-187-3p、miR-1895等;5个miRNA表达下调,包括miR-150-5p、miR-6912-5p、miR-342-5p等。GO分析结果显示,靶基因的功能主要涉及突触、转录因子活性、离子结合、蛋白结合等。KEGG分析结果显示,靶基因富集的通路包括叉头框蛋白O(forkhead box protein O,FoxO)信号通路、胰岛素抵抗、糖尿病并发症中的晚期糖基化终产物及其受体(advanced glycation end product-receptor,AGE-RAGE)信号通路等。结论:益糖康可治疗小鼠糖尿病,其机制可能与调节外周血miRNA表达,影响细胞凋亡、氧化应激、糖脂代谢等功能,调控FoxO信号通路、胰岛素抵抗等通路有关。展开更多
Over the last decade, sequencing of different genomes re- vealed that an increase in organismal complexity is not merely explained by a dramatic increase in the number of protein-coding genes. However, the gradual inc...Over the last decade, sequencing of different genomes re- vealed that an increase in organismal complexity is not merely explained by a dramatic increase in the number of protein-coding genes. However, the gradual increase in protein diversity contributes a lot to the complexity of high- er organisms [1]. It is now widely accepted that non-coding RNAs （ncRNAs）, especially microRNAs （miRNAs） largely define eukaryotic cell functions and the impacts of a variety of gene regulation [2].展开更多
文摘目的:基于高通量测序技术探讨益糖康对糖尿病小鼠外周血miRNA表达谱的影响。方法:从15只C57BL/6小鼠中随机选取5只作为空白组,其余小鼠采用高脂饲料结合腹腔注射链脲佐菌素(100 mg·kg^(-1))的方式建立糖尿病模型。将造模成功的小鼠随机分为模型组和益糖康组(32.2 g·kg^(-1)),每组5只,灌胃9周,每日1次,每周检测空腹血糖(fasting blood glucose,FBG)。采用高通量测序技术检测小鼠外周血miRNA表达情况,筛选差异表达miRNA,并通过miRanda数据库预测靶基因。最后,针对靶基因进行基因本体(Gene Ontology,GO)和京都基因与基因组百科全书(Kyoto Encylopaedia of Genes and Genomes,KEGG)富集分析。结果:给药第1—9周,与空白组比较,模型组小鼠FBG升高(P<0.01);给药第4—9周,与模型组比较,益糖康组小鼠FBG降低(P<0.05,P<0.01)。与模型组比较,益糖康组小鼠外周血8个miRNA表达上调,包括miR-434-3p、miR-187-3p、miR-1895等;5个miRNA表达下调,包括miR-150-5p、miR-6912-5p、miR-342-5p等。GO分析结果显示,靶基因的功能主要涉及突触、转录因子活性、离子结合、蛋白结合等。KEGG分析结果显示,靶基因富集的通路包括叉头框蛋白O(forkhead box protein O,FoxO)信号通路、胰岛素抵抗、糖尿病并发症中的晚期糖基化终产物及其受体(advanced glycation end product-receptor,AGE-RAGE)信号通路等。结论:益糖康可治疗小鼠糖尿病,其机制可能与调节外周血miRNA表达,影响细胞凋亡、氧化应激、糖脂代谢等功能,调控FoxO信号通路、胰岛素抵抗等通路有关。
文摘Over the last decade, sequencing of different genomes re- vealed that an increase in organismal complexity is not merely explained by a dramatic increase in the number of protein-coding genes. However, the gradual increase in protein diversity contributes a lot to the complexity of high- er organisms [1]. It is now widely accepted that non-coding RNAs （ncRNAs）, especially microRNAs （miRNAs） largely define eukaryotic cell functions and the impacts of a variety of gene regulation [2].
