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合成抗菌剂抑制黄曲霉毒素的产生。

Synthetic antimicrobial agents inhibit aflatoxin production.

机构信息

The Guangdong Provincial Key Laboratory for Aquatic Economic Animals, School of Life Sciences, Sun Yat-sen University, Guangzhou, 510275, China.

The Guangdong Provincial Key Laboratory for Biotechnology Drug Candidates, School of Bioscience and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, 510006, China.

出版信息

Braz J Microbiol. 2021 Jun;52(2):821-835. doi: 10.1007/s42770-021-00423-4. Epub 2021 Jan 14.

Abstract

Antimicrobial peptides (AMPs) are biologically active molecules that can eradicate bacteria by destroying the bacterial membrane structure, causing the bacteria to rupture. However, little is known about the extent and effect of AMPs on filamentous fungi. In this study, we synthesized small molecular polypeptides by an inexpensive heat conjugation approach and examined their effects on the growth of Aspergillus flavus and its secondary metabolism. The antimicrobial agents significantly inhibited aflatoxin production, conidiation, and sclerotia formation in A. flavus. Furthermore, we found that the expression of aflatoxin structural genes was significantly inhibited, and the intracellular reactive oxygen species (ROS) level was reduced. Additionally, the antimicrobial agents can change membrane permeability. Overall, our results demonstrated that antimicrobial agents, safe to mammalian cells, have an obvious impact on aflatoxin production, which indicated that antimicrobial agents may be adopted as a new generation of potential agents for controlling aflatoxin contamination.

摘要

抗菌肽(AMPs)是一类具有生物学活性的分子,能够通过破坏细菌的膜结构来杀灭细菌,导致细菌破裂。然而,关于 AMP 对丝状真菌的影响和程度知之甚少。在这项研究中,我们通过一种廉价的热连接方法合成了小分子多肽,并研究了它们对黄曲霉菌生长及其次级代谢的影响。这些抗菌剂显著抑制了黄曲霉菌的产毒、产孢和形成菌核。此外,我们发现,黄曲霉素结构基因的表达受到显著抑制,细胞内活性氧(ROS)水平降低。此外,抗菌剂还可以改变膜通透性。总的来说,我们的研究结果表明,这些对哺乳动物细胞安全的抗菌剂对黄曲霉毒素的产生有明显的影响,这表明抗菌剂可能被用作控制黄曲霉毒素污染的新一代潜在药物。

相似文献

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Synthetic antimicrobial agents inhibit aflatoxin production.合成抗菌剂抑制黄曲霉毒素的产生。
Braz J Microbiol. 2021 Jun;52(2):821-835. doi: 10.1007/s42770-021-00423-4. Epub 2021 Jan 14.
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