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首页> 外文期刊>Biochimica et biophysica acta. Biomembranes >Effect of isoquercitrin on membrane dynamics and apoptosis-like death in Escherichia coli
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Effect of isoquercitrin on membrane dynamics and apoptosis-like death in Escherichia coli

机译：异槲皮素对大肠杆菌膜动力学和凋亡的死亡的影响

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摘要

Abstract Minimum inhibitory concentration (MIC) is defined as the lowest concentration of a compound that completely inhibits microbial growth. Antibacterial mechanisms of compounds have been investigated at their sub-MICs as well as at their MIC. In this study, the effects of sub-MIC and MIC of isoquercitrin on Escherichia coli were investigated. The antibacterial effect of isoquercitrin was tested using the microdilution method. Sub-MICs of isoquercitrin induced the production of reactive oxygen species and depletion of glutathione. The oxidative effects induced by sub-MICs of isoquercitrin could be prolonged, finally resulting in apoptosis-like death. DNA fragmentation and phosphatidylserine externalization, which are regarded as the hallmarks of apoptosis, were evaluated using the TUNEL assay and Annexin V staining, respectively. Furthermore, isoquercitrin induced the peroxidation of membrane lipids and inner membrane permeabilization at both its sub-MIC and MIC. This suggested membrane damage in response to lipid oxidation. The uptake of membrane impermeable dyes, propidium iodide and calcein, demonstrated that isoquercitrin damaged the cell membrane at concentrations higher than its MIC. Thus, isoquercitrin induced apoptosis-like death and dysregulation of cell membrane dynamics. Graphical abstract Display Omitted Highlights ? Isoquercitrin induces the cell death of Escherichia coli cells. ? Isoquercitrin has two antibacterial mechanisms: Apoptosis-like death and Membrane. ? Isoquercitrin has the oxidative effect on E. coli cells. ? Isoquercitrin induces apoptosis-like death at sub-MIC levels. ? Isoquercitrin induces the membrane dysfunction at MIC levels.
机译：摘要最小抑制浓度（MIC）定义为完全抑制微生物生长的化合物的最低浓度。已经在其子MICS以及它们的麦克风中研究了化合物的抗菌机制。在该研究中，研究了亚微米和麦克里林菊体对大肠杆菌的影响。使用微稀释方法测试异槲皮素的抗菌作用。甲状腺素素的亚麦克风诱导了活性氧物种的产生和谷胱甘肽的耗尽。异喹硫脲亚麦克风诱导的氧化效应可以延长，最终导致凋亡样死亡。使用TUNEL测定和附睾v染色评估被视为凋亡标志的DNA碎片和磷脂酰丝氨酸外化。此外，异喹蛋白在其亚麦麦米和麦克风中诱导膜脂质和内膜透化的过氧化。这种建议的膜造成抗脂氧化的损伤。膜不透水染料，碘化丙烯酸铅和碱蛋白的摄取表明，异槲皮素在高于其麦克风的浓度下损坏细胞膜。因此，异喹硫脲诱导细胞凋亡的死亡和细胞膜动力学的失调。图形抽象显示省略了亮点？异喹蛋白诱导大肠杆菌细胞的细胞死亡。还异槲皮素具有两种抗菌机制：凋亡样死亡和膜。还异喹蛋白对大肠杆菌细胞具有氧化作用。还异喹硫序在亚麦麦米德水平下诱导凋亡样死亡。还异喹硫序诱导MIC水平的膜功能障碍。

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