| Summary: | Vulvovaginal candidiasis (VVC) is a common gynecologic disorder caused by fungal infections of the vaginal mucosa, with the most common pathogen being <i>Candida albicans</i> (<i>C. albicans</i>). Exploring metabolite changes in the disease process facilitates further discovery of targets for disease treatment. However, studies on the metabolic changes caused by <i>C. albicans</i> are still lacking. In this study, we used <i>C. albicans</i>-infected vaginal epithelial cells to construct an in vitro model of VVC, analyzed the metabolites by UHPLC-Q-Exactive MS, and screened the potential metabolites based on metabolomics. The results showed that <i>C. albicans</i> infection resulted in significant up-regulation of D-arabitol, palmitic acid, adenosine, etc.; significant down-regulation of lactic acid, nicotinamide (NAM), nicotinate (NA), etc.; and disruption of amino acid metabolism, and that these significantly altered metabolites might be potential therapeutic targets of VVC. Further experiments showed that <i>C. albicans</i> infection led to a decrease in glycolytic enzymes in damaged cells, inhibiting glycolysis and leading to significant alterations in glycolytic metabolites. The present study explored the potential metabolites of VVC induced by <i>C. albicans</i> infection based on metabolomics and verified the inhibitory effect of <i>C. albicans</i> on vaginal epithelial cell glycolysis, which is valuable for the diagnosis and treatment of VVC.
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