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The invasion of Candida albicans is one of the most common fungal infections seen in clinical practice, and serious drug resistance has been reported in recent years. Therefore, new anti-C. albicans drugs must be introduced. In this research, it was demonstrated that cinnamaldehyde (CA) shows strong antimicrobial activity, with 0.26 mg/mL CA being the minimum inhibitory concentration to manage C. albicans. Extraordinarily, we detected that CA accumulated the intracellular reactive oxygen species (ROS) and enhanced the calcium concentration in the cytoplasm and mitochondria through flow cytometry. In addition, we observed that C. albicans cells released Cytochrome c from the mitochondria to the cytoplasm, depolarized the mitochondrial membrane potential, and activated the metacaspase when exposed to 0.065, 0.13, 0.26, and 0.52 mg/mL CA. Furthermore, to confirm that CA introduces the C. albicans apoptosis, we discovered that when the phosphatidylserine was exposed, DNA damage and chromatin condensation occurred, which were detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and 4′,6-diamidino-2-phenylindole (DAPI) staining. Finally, demonstrations of phenotype investigation, colony-forming unit (CFU) counts, and periodic acid–Schiff (PAS) staining were conducted to prove that CA possessed the ability to treat oropharyngeal candidiasis (OPC) and vulvovaginal candidiasis (VVC). From the above, our research indicates that CA is a promising antifungal candidate when applied to C. albicans infections. [ABSTRACT FROM AUTHOR]

Vulvovaginal candidiasis is a common fungal infection afflicting women which is primarily caused by the yeast Candida albicans (C. albicans). It is imperative to introduce new drug classes to counter this threat due to the continuous emergence of drug-resistant cases in recent years. The purpose of this study was to clarify the in vivo antifungal activity of perillaldehyde (PAE) against C. albicans and to prove that PAE is a promising candidate for the control of vaginal candidiasis. An animal model of vaginitis was developed to demonstrate the therapeutic and preventive effects of PAE on vaginal candidiasis, and these were evaluated through fungal and histopathological examinations. In clarifying the mechanism of PAE, standard hematological test results indicated that white blood cells (WBC) were elevated abnormally in mice infected with C. albicans , whereas when the mice were treated with various concentrations of PAE, the number of WBC in the blood was reduced. Flow cytometry was used to detect the populations of neutrophils, macrophages and CD4 T cells in the vaginal tissue of the mice. PAE was found to reduce these immune cells, which all play a key role in the inflammatory response, and the related interleukin and pro-inflammatory cytokines, including IL-17, IL-22 and TNF-α. These were detected using ELISA. Finally, we detected the expression levels of E-cadherin in the PAE treatment mouse group and discovered that it had recovered to its normal levels, but in the infection mouse group, the E-cadherin expression was clearly suppressed by the presence of C. albicans. Our data demonstrated that PAE targets these cytokines and possesses the ability to fight the fungal infection while also reducing the levels of the inflammatory factors identified. Our results demonstrated that PAE has a significant preventative and therapeutic effect on vaginal candidiasis and is a potential candidate for the treatment of vaginal Candida infections. [ABSTRACT FROM AUTHOR]

Perillaldehyde (PAE), a natural monoterpenoid agent extracted from Perilla frutescence , PAE has been reported to present various physiological capabilities, such as anti-inflammation, anti-oxidative and anti-fungal. In this study, we show that PAE exhibits strong antifungal activity against Candida albicans (C. albicans). C. albicans , a fungal pathogen with high incidence of antifungal resistance in clinical settings, is the major cause of oropharyngeal candidiasis (OPC). OPC is characterized by inflammatory immunological responses to fungal infections. Our in vitro results show PAE inhibited several virulence attributes of C. albicans including biofilm formation, yeast-to-hyphal transition and secreted aspartic proteinases (SAPs) gene expression. Using an experimental murine model of OPC, we found that PAE inhibited NLRP3 inflammasome assembly, reduced the excessive accumulation of ROS and prevented the p65 transfer in nuclear; processes all leading to reduced inflammation burden in the host. Together, this supports use PAE as a promising new agent to improve OPC. [ABSTRACT FROM AUTHOR]