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亚油酸-甲硝唑通过氧化抑制 的生长。

Linolenic acid-metronidazole inhibits the growth of through oxidation.

机构信息

School of Basic Medicine, Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China.

School of Basic Medicine, Youjiang Medical University for Nationalities, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China.

出版信息

World J Gastroenterol. 2023 Aug 28;29(32):4860-4872. doi: 10.3748/wjg.v29.i32.4860.

DOI:10.3748/wjg.v29.i32.4860
PMID:37701137
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10494766/
Abstract

BACKGROUND

Resistance to antibiotics is one the main factors constraining the treatment and control of () infections. Therefore, there is an urgent need to develop new antimicrobial agents to replace antibiotics. Our previous study found that linolenic acid-metronidazole (Lla-Met) has a good antibacterial effect against both antibiotic-resistant and sensitive . Also, does not develop resistance to Lla-Met. Therefore, it could be used for preparing broad-spectrum antibacterial agents. However, since the antibacterial mechanism of Lla-Met is not well understood, we explored this phenomenon in the present study.

AIM

To understand the antimicrobial effect of Lla-Met and how this could be applied in treating corresponding infections.

METHODS

cells were treated with the Lla-Met compound, and the effect of the compound on the cell morphology, cell membrane permeability, and oxidation of the bacteria cell was assessed. Meanwhile, the differently expressed genes in in response to Lla-Met treatment were identified.

RESULTS

Lla-Met treatment induced several changes in cells, including roughening and swelling. experiments revealed that Lla-Met induced oxidation, DNA fragmentation, and phosphatidylserine ectropionation in cells. Inhibiting Lla-Met with L-cysteine abrogated the above phenomena. Transcriptome analysis revealed that Lla-Met treatment up-regulated the expression of superoxide dismutase and genes, both anti-oxidation-related genes.

CONCLUSION

Lla-Met kills mainly by inducing oxidative stress, DNA damage, phosphatidylserine ectropionation, and changes on cell morphology.

摘要

背景

抗生素耐药性是限制 () 感染治疗和控制的主要因素之一。因此，迫切需要开发新的抗菌剂来替代抗生素。我们之前的研究发现，亚麻木酚素-甲硝唑（Lla-Met）对 （包括抗生素耐药菌和敏感菌）均具有良好的抗菌作用。而且， 不会对 Lla-Met 产生耐药性。因此，它可以用于制备广谱抗菌剂。然而，由于 Lla-Met 的抗菌机制尚不清楚，我们在本研究中探讨了这一现象。

目的

了解 Lla-Met 的抗菌作用及其在治疗相关感染中的应用。

方法

用 Lla-Met 化合物处理 细胞，评估该化合物对细胞形态、细胞膜通透性和细菌氧化的影响。同时，鉴定了 细胞对 Lla-Met 处理后差异表达的基因。

结果

Lla-Met 处理诱导 细胞发生多种变化，包括粗糙和肿胀。 实验表明，Lla-Met 诱导 细胞氧化、DNA 断裂和磷脂酰丝氨酸外翻。用 L-半胱氨酸抑制 Lla-Met 可消除上述现象。转录组分析显示，Lla-Met 处理上调了超氧化物歧化酶和 基因的表达，这两个基因均与抗氧化有关。

结论

Lla-Met 主要通过诱导氧化应激、DNA 损伤、磷脂酰丝氨酸外翻和细胞形态变化来杀死 。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/61c3cc6f01d3/WJG-29-4860-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/eb8e0a1d0858/WJG-29-4860-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/e98c48cf40d1/WJG-29-4860-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/6f0883723c51/WJG-29-4860-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/f0d3c0536a97/WJG-29-4860-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/ce71a8785072/WJG-29-4860-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/43a5467c46b1/WJG-29-4860-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/61c3cc6f01d3/WJG-29-4860-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/eb8e0a1d0858/WJG-29-4860-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/e98c48cf40d1/WJG-29-4860-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/6f0883723c51/WJG-29-4860-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/f0d3c0536a97/WJG-29-4860-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/ce71a8785072/WJG-29-4860-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/43a5467c46b1/WJG-29-4860-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58d/10494766/61c3cc6f01d3/WJG-29-4860-g007.jpg

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