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As a natural product isolated from thyme oil in thyme, thymol (2‐isopropyl‐5‐methylphenol) harbors antiviral, antioxidant, and other properties, and thus could be potentially used for the treatment of various diseases. However, the function of thymol has not been comprehensively studied. Here, we applied an inverse molecular docking approach to identify unappreciated functions of thymol. Potential targets of thymol in humans were identified by the server of DRAR‐CPI, and targets of interest were then assessed by GO and KEGG pathway analysis. Subsequently, homologous proteins of these targets in Caenorhabditis elegans were identified by Blast tool, and their three‐dimensional structures were achieved using Swiss‐Model workspace. Interaction between thymol and the targeted proteins in worms was verified using AutoDock 4.0. Analyses of the targets revealed that thymol could be potentially involved in the glycolysis/gluconeogenesis and fatty acid degradation pathways. To verify the activity of thymol on lipid deposition in vivo, the C. elegans model was established. The lipid content of nematodes induced by high‐dose glucose was determined by Oil Red O and Nile Red staining, and gene expression was assessed by qRT‐PCR. The results showed that thymol might lead to the acceleration of β‐oxidation by upregulating cpt‐1, aco, fabp, and tph‐1, causing the descent of lipid content in nematodes. Our findings indicated that thymol could be potentially used for the treatment of chronic metabolic diseases associated with increased fatty acid deposition. [ABSTRACT FROM AUTHOR]

Listeria monocytogenes frequently causes Listeriosis in humans and animals. In present study, we discovered that in the presence of FeSO 4 , L. monocytogenes became viable but non-culturable (VBNC), and remained virulent to Caenorhabditis elegans. The killing assay indicated that these VBNC cells kept sensitive to tetracycline, differing from dormant cells. Transcriptomic analysis revealed more gene transcription occurrence in the VBNC cells compared to dormant cells, involving stress response and ribosome binding. No ferroptosis hallmarks were observed in the VBNC cells, whereas the application of either intracellular Fe2+ chelator or the ferroptosis inhibitor arrested the formation of VBNC state by FeSO 4 , as well as by Benzakonium chloride or Haz-Tab. This implicated the universal involvement of intracellular Fe2+ and other cascades related to ferroptosis in the formation of VBNC state in L. monocytogenes. Taken together, we discovered an iron-induced VBNC state in L. monocytogenes , and provided clues to further understanding their potential risks. [ABSTRACT FROM AUTHOR]