Abstract
Infectious diseases caused by drug-resistant Escherichia coli (E. coli) pose a critical concern for medical institutions as they can lead to high morbidity and mortality rates. In this study, amygdalin exhibited anti-inflammatory and antioxidant activities, as well as other potentials. However, whether it could influence the drug-resistant E. coli-infected cells remained unanswered. Amygdalin was therefore tested in a cellular model in which human macrophages were exposed to resistant E. coli. Apoptosis was measured by flow cytometry and the lactate dehydrogenase (LDH) assay. Western immunoblotting and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were used to quantify interleukin-18 (IL-18), interleukin-1β (IL-1β), and interleukin-6 (IL-6). The production of reactive oxygen species (ROS) in macrophages was detected by ROS kit. The expression of panapoptotic proteins in macrophages was measured by qRT-PCR and western immunoblotting. Drug-resistant E. coli inhibited cell viability and enhanced apoptosis in the cellular model. In amygdalin-treated cells, amygdalin can inhibit cell apoptosis and pro-inflammatory cytokine expression of IL-1β, IL-18, and IL-6, and it reduces the production of pan-apoptotic proteins. In addition, amygdalin reduced the levels of E. coli-induced ROS in cells, indicating that it has antioxidant effects. Amygdalin, a compound with a protective role, alleviated cell damage caused by drug-resistant E. coli in human macrophages by inhibiting the PANoptosis signaling pathway.
Published Version
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