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金纳米颗粒在大肠杆菌中诱导一种不依赖于活性氧物质的凋亡途径。

Gold nanoparticles induce a reactive oxygen species-independent apoptotic pathway in Escherichia coli.

机构信息

School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, Daehakro 80, Bukgu, Daegu 41566, Republic of Korea.

School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, Daehakro 80, Bukgu, Daegu 41566, Republic of Korea.

出版信息

Colloids Surf B Biointerfaces. 2018 Jul 1;167:1-7. doi: 10.1016/j.colsurfb.2018.03.049. Epub 2018 Mar 30.

DOI:10.1016/j.colsurfb.2018.03.049
PMID:29625418
Abstract

Gold nanoparticles (AuNPs) are a promising material for use in biological and biotechnological applications. While applications such as drug delivery, sensory probe, and organic photovoltaics have been widely evaluated, studies of the antimicrobial activity of AuNPs in therapeutic agents are lacking. In this study, the antibacterial activity and mode of action of AuNPs on Escherichia coli was focused. The membrane-impermeable dye SYTOX green was not taken up and membrane potential was depolarized by AuNPs. This demonstrated that AuNPs inhibit cell growth without directly causing membrane damage. Depolarization of membrane potential results in calcium uptake and processes such as bacterial apoptotic-like cell death. We confirmed that AuNPs induced DNA fragmentation resulting in apoptosis-like cell death in a TUNEL assay. FITC-VAD-FMK showed that caspase-like protein(s) such as RecA were activated, induced, and overexpressed. Additionally, elevated levels of intracellular reactive oxygen species (ROS) and decreased reduced glutathione were observed. In AuNP-treated cells, ROS elevation was not confirmed; however, glutathione was decreased. Based on these observations, AuNPs induce apoptotic-like death by severely damaging DNA and this was independent of ROS in E. coli.

摘要

金纳米粒子(AuNPs)是一种很有前途的材料,可用于生物和生物技术应用。虽然已经广泛评估了其在药物输送、传感探针和有机光伏等方面的应用,但关于 AuNPs 作为治疗剂的抗菌活性的研究还很少。在本研究中,重点研究了 AuNPs 对大肠杆菌的抗菌活性和作用模式。膜不可渗透的染料 SYTOX green 没有被摄取,并且 AuNPs 使膜电位去极化。这表明 AuNPs 抑制细胞生长而不会直接导致膜损伤。膜电位去极化导致钙摄取和类似细菌凋亡的细胞死亡等过程。我们通过 TUNEL 测定证实 AuNPs 诱导了 DNA 片段化,导致类似凋亡的细胞死亡。FITC-VAD-FMK 表明,RecA 等半胱天冬酶样蛋白被激活、诱导和过表达。此外,还观察到细胞内活性氧(ROS)水平升高和还原型谷胱甘肽减少。在 AuNP 处理的细胞中,未确认 ROS 升高;然而,谷胱甘肽减少。基于这些观察结果,AuNPs 通过严重破坏 DNA 诱导类似凋亡的死亡,这在大肠杆菌中与 ROS 无关。

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