目的从印度洋深海沉积物中分离可培养海洋放线菌,对获得的一株海洋微生物进行抗革兰阴性菌活性物质研究。方法设计11种分离培养基进行海洋放线菌分离,通过16S r RNA基因序列比对分析确定菌株分类;利用多种色谱方法,对菌株IMB16-059产生...
详细信息
目的从印度洋深海沉积物中分离可培养海洋放线菌,对获得的一株海洋微生物进行抗革兰阴性菌活性物质研究。方法设计11种分离培养基进行海洋放线菌分离,通过16S r RNA基因序列比对分析确定菌株分类;利用多种色谱方法,对菌株IMB16-059产生的活性物质进行分离纯化,通过波谱学和化学方法鉴定其结构。结果根据菌落表型共分离得68株微生物,经16S r RNA分析表明,其中34株属于放线菌门,覆盖5科5属;其余属于厚壁菌门和变形菌门。25株发酵产物显示出抗革兰阴性菌活性。从赤杆菌IMB16-059中分离鉴定了6个化合物,其结构分别确定为L,L-环(脯氨酸-丙氨酸)(1),L,L-环(脯氨酸-酪氨酸(2)),D,L-环(脯氨酸-酪氨酸)(3),邻氨基苯甲酸(4),胸腺嘧啶(5),1H-喹啉-4-酮(6)。化合物1和4显示出抗铜绿假单胞菌活性,在样品浓度为20μg/片时,抑菌圈直径分别为13和20mm。结论印度洋深海沉积物蕴含丰富的微生物类群,其发酵产物显示出较好的抗革兰阴性菌活性,可为新抗生素发现提供重要的菌种资源。
Type 2 diabetes mellitus is characterized by insulin ***,the complete molecular mechanism remains *** this study,zebrafish were fed a long-term highfat diet to induce type 2 diabetes,which resulted in a higher body we...
详细信息
Type 2 diabetes mellitus is characterized by insulin ***,the complete molecular mechanism remains *** this study,zebrafish were fed a long-term highfat diet to induce type 2 diabetes,which resulted in a higher body weight,body mass index,more lipid vacuoles in liver,increased insulin transcription level in liver,brain and muscle,and high fasting blood glucose in the high-fat diet ***,the transcription levels of insulin substrate-2 and glucose transporter 2 were significantly decreased,indicating insulin signaling pathway and glucose transport impaired in the insulin-targeting *** of the autophagy-related genes,ATG3,ATG4B,ATG5,ATG7 and ATG12 were decreased but autophagy inhibitor gene m-TOR increased,and autophagyflux was inhibited in liver of the high-fat diet *** changes were confirmed in palmitic acid-treated HepG2 ***,in co-immunoprecipitation and subcellular colocalization experiments,the conjunction of preproinsulin with cargo-recognition protein p62 increased,but conjuncts of autophagosome with p62-cargo,lysosomes with p62-cargo,and autolysosomes decreased ***,lysosomes,autolysosomes and conjuncts of p62-insulin localized at the periphery of palmitic acid-treated cells,the margination of lysosomes may mediate deactivation of proteases *** findings suggest that intracellular high-lipid may trigger defective autophagy,impaired downstream signaling of insulin and accumulated intracellular preproinsulin,leading to dysregulation of cell homeostasis mechanism,which may be one of reasons involved in insulin-resistance in type 2 diabetes.
暂无评论