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萘醌类化合物抑制肠道耶尔森氏菌生物膜的形成和生存能力。

Naphthoquinones inhibit formation and viability of Yersinia enterocolitica biofilm.

机构信息

Instituto de Investigación en Tecnología Química- Consejo Nacional de Investigaciones Científicas y Técnicas (INTEQUI- CONICET), San Luis, Argentina.

Química Orgánica, Facultad de Química, Bioquímica y Farmacia, Universidad Nacional de San Luis, San Luis, Argentina.

出版信息

World J Microbiol Biotechnol. 2021 Jan 18;37(2):30. doi: 10.1007/s11274-020-02971-7.

Abstract

The capacity of different naphthoquinones to inhibit and eradicate Yersinia enterocolitica biofilm was investigated and possible mechanisms of action were evaluated. Inhibition of biofilm formation and cell viability, quorum sensing (QS) inhibition and oxidative stress generation of 23 naphthoquinones were assayed against Yersinia enterocolitica. The best anti-biofilm agents at 100 µmol l were compounds 3, 11 and 13, which showed biofilm inhibition higher than 75%. Compound 3 was the most effective against biofilm forming capacity of Y. enterocolitica WAP 314 with a minimum biofilm inhibitory concentration (MBIC) of 25 µmol l; while against Y. enterocolitica CLC001, the lowest MBIC was 6.1 µmol l for compound 11. Acyl-homoserine lactones production was decreased with compound 13. We showed that the oxidative stress influence biofilm growth, by means of ROS and RNI increment. All treatments increased ROS and RNI values in the biofilm of both strains; while in planktonic cells, the increase was lesser. Additionally, Y. enterocolitica WAP 314 biofilm treated with compounds 11 and 13 showed above 80% of SOD consumption. In Y. enterocolitica CLC001 biofilm all compounds induced above 90% of SOD consumption. The SOD activity was higher in biofilm than in planktonic cells. In conclusion, this is the first study to demonstrate that naphthoquinones are able to inhibit biofilm formation of Y. enterocolitica without critical disturbing its planktonic growth. Naphthoquinones as anti-biofilm agents might potentially be useful in the treatment of biofilm-associated infections in the future.

摘要

本研究考察了不同萘醌对肠耶尔森氏菌生物膜的抑制和清除作用,并评估了可能的作用机制。采用微量稀释法检测了 23 种萘醌对肠耶尔森氏菌的生物膜形成抑制率和细胞活力、群体感应(QS)抑制率及氧化应激水平。在 100 μmol/L 浓度下,化合物 3、11 和 13 对生物膜的抑制率最高,均高于 75%。化合物 3 对 WAP 314 的最小生物膜抑制浓度(MBIC)为 25 μmol/L,对 WAP 314 的生物膜抑制效果最好;而对 CLC001 的 MBIC 最低,为 6.1 μmol/L。化合物 13 能减少酰基高丝氨酸内酯的产生。我们通过 ROS 和 RNI 的增加证明了氧化应激对生物膜生长的影响。所有处理均使两种菌株的生物膜中 ROS 和 RNI 值增加;而在浮游细胞中,增加量较小。此外,用化合物 11 和 13 处理 WAP 314 生物膜后,SOD 消耗超过 80%。在 CLC001 生物膜中,所有化合物均诱导 SOD 消耗超过 90%。生物膜中的 SOD 活性高于浮游细胞。综上所述,这是首次证明萘醌能够抑制肠耶尔森氏菌生物膜的形成,而不会对其浮游生长造成严重干扰。未来,萘醌类化合物作为抗生物膜药物可能具有治疗生物膜相关感染的潜力。

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