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tachyplesin I 在大肠杆菌中诱导类似细胞凋亡的死亡特性。

Apoptosis-like death-inducing property of tachyplesin I in Escherichia coli.

机构信息

School of Life Sciences, BK 21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Republic of Korea.

出版信息

J Basic Microbiol. 2021 Sep;61(9):795-807. doi: 10.1002/jobm.202100133. Epub 2021 Aug 1.

Abstract

Antimicrobial peptide (AMP) derived from the horseshoe crab, tachyplesin I (KWCFRVCYRGICYRRCR-NH ), displayed the apparent antimicrobial activity with low cytotoxicity, suggesting its efficacy as an attractive agent but still lacks the understandings regarding its mechanism(s). Hence, the study focused on investigating the antibacterial mode of action of tachyplesin I against Escherichia coli. Based on the reactive oxygen species generation displayed in several antimicrobial effects, the detection of superoxide anion and nitric oxide were verified after tachyplesin I treatment. Substantial increment of two molecules was followed by the imbalance in intracellular ion concentration, noticeably magnesium and calcium. The series of stages led to hydroxyl radical generation with reduced glutathione, followed by damage in DNA due to oxidative stress. Eventually, the apoptosis-like death in E. coli was monitored in DNA fragmentation-dependent manner due to the tachyplesin I treatment, verified by membrane depolarization, caspase-like protein activation, and phosphatidylserine exposure. Accordingly, tachyplesin I induces apoptosis-like death in E. coli, suggesting the potential of being a candidate for regulating bacterial infection.

摘要

抗菌肽(AMP)来源于鲎,其序列为 tachyplesin I(KWCFRVCYRGICYRRCR-NH),具有明显的抗菌活性和低细胞毒性,表明其作为一种有吸引力的药物具有潜在的功效,但对其作用机制仍缺乏了解。因此,本研究集中于研究 tachyplesin I 对大肠杆菌的抗菌作用模式。基于几种抗菌作用中显示的活性氧生成,在 tachyplesin I 处理后验证了超氧阴离子和一氧化氮的产生。两种分子的大量增加伴随着细胞内离子浓度的失衡,特别是镁和钙。一系列的阶段导致了由于氧化应激导致谷胱甘肽产生的羟基自由基,最终由于 tachyplesin I 的处理导致了 DNA 的损伤。最终,通过膜去极化、半胱天冬酶样蛋白激活和磷脂酰丝氨酸暴露,以依赖于 DNA 片段化的方式监测了大肠杆菌中的凋亡样死亡。因此,tachyplesin I 诱导大肠杆菌中的凋亡样死亡,表明其可能成为调节细菌感染的候选药物。

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