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群体感应抑制剂(QSIs)具有不会产生抗药性的特点，从而被作为抗生素的可能替代品，具有广阔的应用前景，因此其存在着与传统抗生素环境联合暴露的可能，但是目前尚缺乏相关联合效应的研究。本文以大肠杆菌(Escherichia coli)为受试生物，测定了7种QSIs(DL-焦谷氨酸、N-乙烯基吡咯烷酮、呋喃酮乙酸酯、2-甲基四氢呋喃-3-酮、3,4-二溴-2(5H)-呋喃酮、(R)-3-吡咯烷醇、D-脯氨醇)分别与磺胺甲恶唑(SMX)和盐酸强力霉素(DH)的二元联合毒性，并初步探讨了它们的联合作用机制。根据结果分析，前5种QSIs作用于AI-2类信号分子介导的群体感应系统，与AI-2类信号分子竞争结合LsrB蛋白，此通路与SMX、DH的作用通路互不影响，因此联合效应为相加；后2种QSIs作用于AI-1类信号分子介导的群体感应系统，与AI-1类信号分子竞争结合SdiA蛋白，而SMX、DH的作用可能刺激SdiA蛋白的表达，从而需要消耗更多的QSIs与SdiA结合，因而联合效应为拮抗。本实验研究可为传统抗生素与QSIs联合暴露的生态风险评价提供一定理论基础。
QSIs are not drug-resistant, so they have potential applications as antibiotics. Therefore, QSIs may be exposed in combination with traditional antibiotics, but there is no relevant association Study of effects. In this paper, seven kinds of QSIs (DL-pyroglutamic acid, N-vinyl pyrrolidone, furanone acetate, 2-methyltetrahydrofuran-3-one, Binary combination of Sulfamethoxazole (SMX) and Doxycycline Hydrochloride (DH) with 4-dibromo-2 (5H) -furanone, (R) -3-pyrrolidinol and D- Toxicity, and initially discussed their joint mechanism of action. According to the results, the first five QSIs act on the population-sensing system mediated by AI-2 signaling molecules and compete with the AI-2 signaling molecules for binding to LsrB protein. This pathway has no effect on the pathway of interaction with SMX and DH, The latter two QSIs act on the population-sensing system mediated by AI-1 signaling molecule and compete with AI-1 signaling molecules for binding to SdiA protein. The effect of SMX and DH may stimulate SdiA protein expression Consumption of more QSIs needs to be combined with SdiA and thus the combined effect is antagonistic. The experimental study may provide a theoretical basis for the ecological risk assessment of traditional antibiotics and QSIs exposure.