大蒜素分解产物二烯丙基二硫对小鼠急性肝损伤的保护作用

目的 研究大蒜活性物质二烯丙基二硫(diallyl disulfide, DADS)对四氯化碳诱导的小鼠急性肝损伤的保护作用及其机制。方法 将36只Balb/c小鼠随机分为4组,分别为正常组、模型组、阳性组和DADS组。测定小鼠体质量与肝脏指数、天门冬氨酸氨基转移酶(aspartate aminotransferase, AST)、碱性磷酸酶(alkaline phosphatase, ALP)、总超氧化物歧化酶(superoxide dismutase, SOD)、丙二醛(malonaldehyde, MDA)水平,观察肝脏病理学变化;将肝脏样品进行转录组测序,确定差异基因行使的主要生物学功能;将盲肠内容物进行16s rRNA测序,在各个分类水平上进行群落结构的统计分析。结果 DADS可以显著降低四氯化碳肝损伤小鼠肝脏指数,降低AST、ALP活力,提高SOD活力;减少肝脏组织损伤面积、细胞坏死、炎细胞浸润;转录组学分析显示有130个差异表达基因,基因本体论联合会建立的数据库(gene ontology, GO)富集分析显示这些差异基因主要涉及类固醇代谢过程、脂质代谢过程、胆固醇代谢过程,京都基因与基因组百科全书(kyoto encyclopedia of genes and genomes, KEGG)富集分析显示这些差异基因主要涉及类固醇生物合成、视黄醇代谢、药物代谢-细胞色素P450和胆汁分泌等通路。16s rRNA测序结果显示,DADS处理增加了肝损伤小鼠的厚壁菌门、norank_f_Muribaculaceae、Lachnospiraceae_NK4A136_group的相对丰度,降低了变形菌门、Escherichia-Shigella的相对丰度。结论 DADS具有较强的抗四氯化碳肝损伤的潜力,其机制可能是通过提高体内抗氧化水平、调控类固醇代谢相关基因、调节胆汁酸代谢和肠道菌群组成。     

Transcriptome Analysis in a Primary Human Muscle Cell Differentiation Model for Myotonic Dystrophy Type 1

Myotonic dystrophy type 1 (DM1) is caused by CTG-repeat expansions leading to a complex pathology with a multisystemic phenotype that primarily affects the muscles and brain. Despite a multitude of information, especially on the alternative splicing of several genes involved in the pathology, information about additional factors contributing to the disease development is still lacking. We performed RNAseq and gene expression analyses on proliferating primary human myoblasts and differentiated myotubes. GO-term analysis indicates that in myoblasts and myotubes, different molecular pathologies are involved in the development of the muscular phenotype. Gene set enrichment for splicing reveals the likelihood of whole, differentiation stage specific, splicing complexes that are misregulated in DM1. These data add complexity to the alternative splicing phenotype and we predict that it will be of high importance for therapeutic interventions to target not only mature muscle, but also satellite cells.     

酵母菌高糖耐受机制的研究进展

在酒精浓醪发酵生产中,酵母菌在高糖度、高渗透压等恶劣环境下发酵产生乙醇的性能与其耐受机制有密切的联系。该文以酵母菌高糖耐受机制为切入点,介绍了耐高糖酵母菌的来源,高糖胁迫下酵母菌的应激反应,归纳已公开报道的与酵母菌高糖耐受机制可能有关的基因,借鉴真菌及细菌在转录组学与蛋白质组学水平上耐受性能及机制的研究,为基因水平上酵母菌高糖耐受机制的相关研究提供参考。