食品科学 ›› 2026, Vol. 47 ›› Issue (12): 1-12.doi: 10.7506/spkx1002-6630-20260106-040

• 基础研究 •    

槐米多酚抑制大肠杆菌的机理分析

黑俊肖,芦姝羽,闫栋,吴雪,王鑫,李雨欣,海丹,黄现青,沈玥   

  1. (1.河南农业大学食品科学技术学院,河南 郑州 450002;2.河南省食品加工流通安全控制工程研究中心,河南 郑州 450002)
  • 发布日期:2026-07-08
  • 基金资助:
    河南省重点研发计划项目(241111110600);河南省研究生联合培养基地项目(YJS2022JD16); 河南省科技副总项目(HNFZ20240328);河南省高校科技创新团队支持计划项目(23IRTSTHN023)

Inhibition Mechanism of Escherichia coli by Polyphenols from Flos Sophorae Immaturus

HEI Junxiao, LU Shuyu, YAN Dong, WU Xue, WANG Xin, LI Yuxin, HAI Dan, HUANG Xianqing, SHEN Yue   

  1. (1. College of Food Science and Technology, Henan Agricultural University, Zhengzhou 450002, China; 2. Henan Province Engineering Research Center for Food Safety Control of Processing and Circulation, Zhengzhou 450002, China)
  • Published:2026-07-08

摘要: 本研究以非致病性大肠杆菌(Escherichia coli)标准模式菌株ATCC 25922为研究对象,通过高效液相色谱分析槐米多酚的化合物组成及含量,并探究其抑菌活性。研究从大肠杆菌形态特征、物质代谢和氧化应激等多方面阐释槐米多酚的抑菌机制,并利用分子对接技术验证其抑菌机理。结果表明,槐米多酚提取物含有10 种多酚成分,对大肠杆菌具有显著的抑菌活性,其最小抑菌浓度(minimum inhibitory concentration,MIC)和最小杀菌浓度分别为12.5 mg/mL和100 mg/mL,且呈现浓度依赖性效应。抑菌机制研究表明,在MIC条件下,槐米多酚主要通过破坏细胞膜和细胞壁结构并降低其抗性,同时抑制RNA、脂肪和蛋白质合成,最终导致细菌死亡,其可能靶向大肠杆菌的3-羟基酰基-ACP脱水酶和DNA结合转录抑制因子蛋白。在2 MIC和4 MIC条件下,槐米多酚主要通过诱导细菌产生大量的活性氧和丙二醛,进而破坏膜结构和功能,并抑制RNA、蛋白质及肽聚糖合成,从而降低细菌抗性并致其死亡,可能靶向2,5-二酮-D-葡萄糖酸还原酶A蛋白。本研究可为槐米多酚后续靶向食源性致病大肠杆菌的应用研究奠定基础,并为多酚类天然抑菌剂的开发提供理论依据。

关键词: 槐米多酚提取物;大肠杆菌;抑菌机制;抗性

Abstract: In this study, the composition and content of polyphenols in Flos Sophorae Immaturus (FSI) were analyzed by high performance liquid chromatography (HPLC), and their antibacterial activity against the non-pathogenic standard type strain Escherichia coli ATCC 25922 was explored. Additionally, the antibacterial mechanism was elucidated from multiple aspects, including cell wall and membrane alterations, morphological characteristics, metabolic pathways, and oxidative stress responses in E. coli, and it was verified by molecular docking analysis. The results showed that the polyphenol extract contained 10 polyphenolic compounds and exhibited significant antibacterial activity against E. coli. Its minimum inhibitory concentration (MIC) and minimum bactericidal concentration were 12.5 and 100 mg/mL, respectively, and this effect was concentration-dependent. The mechanistic study demonstrated that at MIC, FSI polyphenols mainly damaged the cell membrane and cell wall integrity and reduced their resistance. Simultaneously, these compounds inhibited the biosynthesis of RNA, lipid and protein, ultimately resulting in bacterial cell death. Moreover, FSI polyphenols potentially targeted the 3-hydroxyacyl-[acyl-carrier-protein] dehydratase (fabZ) and acriflavine resistance regulator (acrR) proteins in E. coli. At 2 MIC and 4 MIC, FSI polyphenols mainly triggered excessive accumulation of reactive oxygen species (ROS) and malondialdehyde (MDA), disrupted membrane structure and function, inhibited the synthesis of RNA, protein and peptidoglycan, reduced bacterial resistance, and ultimately caused bacterial death. Furthermore, FSI polyphenols may target the 2,5-diketo-D-gluconic acid reductase A (dkgA) protein in E. coli. This study lays the basis for the application of FSI polyphenols as an antibacterial agent against foodborne pathogenic E. coli, and provides theoretical support the development of polyphenol-based natural antibacterial agents.

Key words: polyphenol extract from Flos Sophorae Immaturus; Escherichia coli; bacteriostasis mechanism; resistance

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