Licochalcone A Protects Vaginal Epithelial Cells Against Candida albicans Infection Via the TLR4/NF-κB Signaling Pathway

• Published in: The journal of microbiology 2024, 62(7), , pp.525-533
• Main Authors: Li, Wei, Yin, Yujun, Li, Taoqiong, Wang, Yiqun, Shi, Wenyin
• Format: Article
• Language: English
• Subjects: Adhesion; Antifungal Agents - pharmacology; Assaying; BAX protein; Bcl-2 protein; biofilm; Biofilms; Biofilms - drug effects; Biomedical and Life Sciences; Candida albicans; Candida albicans - drug effects; Candida albicans - physiology; Candidiasis; Candidiasis, Vulvovaginal - microbiology; Cell Line; Cells; Chalcones - pharmacology; Cholecystokinin; Cytokines; Cytotoxicity; Damage assessment; Down-regulation; ELISA; Enzyme-linked immunosorbent assay; Epithelial cells; Epithelial Cells - drug effects; Epithelial Cells - metabolism; Epithelial Cells - microbiology; Epithelium; Female; Fluorescence; Genomics and Molecular Biology; Humans; Infections; Inflammation; Licochalcone A; Life Sciences; Microbial Genetics; Microbiology; Molecular modelling; NF-kappa B - metabolism; NF-κB protein; protein synthesis; secretion; Signal transduction; Signal Transduction - drug effects; therapeutics; TLR4 protein; Toll-like receptor 4; Toll-Like Receptor 4 - metabolism; Toll-like receptors; Vagina; Vagina - microbiology; vulvovaginal candidiasis; Western blotting; 생물학
• ISSN: 1225-8873; 1976-3794; 1976-3794
• DOI: 10.1007/s12275-024-00134-z

Vulvovaginal candidiasis (VVC) is a prevalent condition affecting a significant portion of women worldwide. Licochalcone A (LA), a natural compound with diverse biological activities, holds promise as a protective agent against Candida albicans ( C. albicans ) infection. This study aims to investigate the potential of LA to safeguard vaginal epithelial cells (VECs) from C. albicans infection and elucidate the underlying molecular mechanisms. To simulate VVC in vitro, VK2-E6E7 cells were infected with C. albicans . Candida albicans biofilm formation, C. albicans adhesion to VK2-E6E7 cells, and C. albicans -induced cell damage and inflammatory responses were assessed by XTT reduction assay, fluorescence assay, LDH assay, and ELISA. CCK-8 assay was performed to evaluate the cytotoxic effects of LA on VK2-E6E7 cells. Western blotting assay was performed to detect protein expression. LA dose-dependently hindered C. albicans biofilm formation and adhesion to VK2-E6E7 cells. Furthermore, LA mitigated cell damage, inhibited the Bax/Bcl-2 ratio, and attenuated the secretion of pro-inflammatory cytokines in C. albicans -induced VK2-E6E7 cells. The investigation into LA’s impact on the Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) pathway revealed that LA downregulated TLR4 expression and inhibited NF-κB activation in C. albicans -infected VK2-E6E7 cells. Furthermore, TLR4 overexpression partially abated LA-mediated protection, further highlighting the role of the TLR4/NF-κB pathway. LA holds the potential to safeguard VECs against C. albicans infection, potentially offering therapeutic avenues for VVC management.