Activity of 6-methoxydihydrosanguinarine from Hylomecon japonica against wild-type and fluconazole-resistant Candida albicans biofilms.

The threat posed by microorganisms to food safety in development necessitates the discovery of new antimicrobial agents. Here, we unravel the antifungal activity of 6-methoxydihydrosanguinarine (6-ME) derived from Hylomecon japonica. 6-ME disrupted the biofilm formation of Candida albicans (C. albicans). 6-ME could cause the blockage of filamentation and classical cyclic adenosine monophosphate (cAMP) signaling pathway is involved in this process. 6-ME downregulated the expression of EFG1, CDC35, RAS1, and TPK2, all of which are critical components of the cAMP pathway. Furthermore, 6-ME changed the membrane permeability of C. albicans and caused reactive oxygen species accumulation, leading to cell death.