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杀菌金纳米粒子对大肠杆菌作用的分子机制。

The molecular mechanism of action of bactericidal gold nanoparticles on Escherichia coli.

机构信息

State Key Laboratory of Bioelectronics, School of Biological Science and Medical Engineering, Southeast University, 2 Si Pailou, Nanjing 210096, China.

出版信息

Biomaterials. 2012 Mar;33(7):2327-33. doi: 10.1016/j.biomaterials.2011.11.057. Epub 2011 Dec 17.

DOI:10.1016/j.biomaterials.2011.11.057
PMID:22182745
Abstract

This work examines the molecular mechanism of action of a class of bactericidal gold nanoparticles (NPs) which show potent antibacterial activities against multidrug-resistant Gram-negative bacteria by transcriptomic and proteomic approaches. Gold NPs exert their antibacterial activities mainly by two ways: one is to collapse membrane potential, inhibiting ATPase activities to decrease the ATP level; the other is to inhibit the subunit of ribosome from binding tRNA. Gold NPs enhance chemotaxis in the early-phase reaction. The action of gold NPs did not include reactive oxygen species (ROS)-related mechanism, the cause for cellular death induced by most bactericidal antibiotics and nanomaterials. Our investigation would allow the development of antibacterial agents that target the energy-metabolism and transcription of bacteria without triggering the ROS reaction, which may be at the same time harmful for the host when killing bacteria.

摘要

本研究通过转录组学和蛋白质组学方法,研究了一类杀菌金纳米粒子(NPs)的作用机制。这类纳米粒子对多种耐药革兰氏阴性菌具有很强的抗菌活性。金纳米粒子主要通过两种方式发挥其抗菌活性:一是破坏膜电位,抑制 ATP 酶活性,降低 ATP 水平;另一种是抑制核糖体亚基与 tRNA 的结合。金纳米粒子增强了趋化作用的早期反应。金纳米粒子的作用不包括活性氧(ROS)相关机制,这是大多数杀菌抗生素和纳米材料诱导细胞死亡的原因。我们的研究将允许开发针对细菌能量代谢和转录的抗菌药物,而不会引发 ROS 反应,当杀死细菌时,这可能对宿主同时有害。

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