Microbial pathogenesis · 2025
Fungicidal effects of saponin extract from rhizomes of Dioscorea panthaica Prain et Burk involve cell membrane damages in Candida glabrata.
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Li Wenmao, Zhang Yanfeng, Zhuang Xinming, Ma Zhiming, Sui Yujie, Yang Longfei
Аннотация
BACKGROUND: Antifungal resistance is increasing worldwide, which is exacerbating the serious conditions faced by the public healthcare system: there are only a few kinds of antifungal drugs. It is pressing to identify new antifungal agents and therapies to prevent and treat fungal infections, especially those caused by resistant Candida species, such as Candida glabrata. This study was to explore the antifungal effects of saponin extract from rhizomes of Dioscorea panthaica Prain et Burk (HSE, abbreviated from the commercial name Huangshanyao Saponin Extract) on the growth, biofilm formation of C. glabrata and its preliminary mechanism.
METHODS: The minimum inhibitory concentration (MIC) of HSE against C. glabrata and other Candida species were evaluated following the guidelines of CLSC-M27-A3. The minimum fungicide concentration (MFC) were defined as the lowest concentration of HSE that caused no colony grown on SD agar after 48-h culture. The effects of HSE on biofilm formation and development were determined through XTT reduction assays. Confocal laser scanning microscope (CLSM) was employed to detect the influence of HSE on biofilm formation, cell membrane permeability and cell membrane potential of C. glabrata. Transmission electron microscope (TEM) was also employed to detect the ultrastructural changes caused by HSE. Checkerboard assays were performed to detect the interactions between HSE and antifungal drugs.
RESULTS: HSE inhibited the growth of C. glabrata and C. albicans, as well as C. parapsilosis, with MIC of 32, 32 and 64 μg/mL, respectively. The MFC of HSE against C. glabrata and C. albicans were 32 or 64 μg/mL. While the MFC against C. parapsilosis was above 512 μg/mL. The adhesion, biofilm formation and development could also be inhibited by HSE. HSE caused cell membrane damages, as revealed by confocal microscopic analysis of PI staining and DiBAC4(3) staining. Results from TEM observation also confirmed the damages of cell membrane. In addition, HSE can synergize with AmB, while CAS and HSE can produce synergistic or additive effects.
CONCLUSION: HSE showed antifungal activities against C. glabrata, as well as Candida parapsilosis, and inhibited C. glabrata biofilm formation and development. Its antifungal mechanism involves the increase in cell membrane permeability. HSE potentiated AmB and caspofungin in C. glabrata, C. parapsilosis and C. albicans. Our results suggested that HSE may be explored as antifungal agents to control Candida infections.
METHODS: The minimum inhibitory concentration (MIC) of HSE against C. glabrata and other Candida species were evaluated following the guidelines of CLSC-M27-A3. The minimum fungicide concentration (MFC) were defined as the lowest concentration of HSE that caused no colony grown on SD agar after 48-h culture. The effects of HSE on biofilm formation and development were determined through XTT reduction assays. Confocal laser scanning microscope (CLSM) was employed to detect the influence of HSE on biofilm formation, cell membrane permeability and cell membrane potential of C. glabrata. Transmission electron microscope (TEM) was also employed to detect the ultrastructural changes caused by HSE. Checkerboard assays were performed to detect the interactions between HSE and antifungal drugs.
RESULTS: HSE inhibited the growth of C. glabrata and C. albicans, as well as C. parapsilosis, with MIC of 32, 32 and 64 μg/mL, respectively. The MFC of HSE against C. glabrata and C. albicans were 32 or 64 μg/mL. While the MFC against C. parapsilosis was above 512 μg/mL. The adhesion, biofilm formation and development could also be inhibited by HSE. HSE caused cell membrane damages, as revealed by confocal microscopic analysis of PI staining and DiBAC4(3) staining. Results from TEM observation also confirmed the damages of cell membrane. In addition, HSE can synergize with AmB, while CAS and HSE can produce synergistic or additive effects.
CONCLUSION: HSE showed antifungal activities against C. glabrata, as well as Candida parapsilosis, and inhibited C. glabrata biofilm formation and development. Its antifungal mechanism involves the increase in cell membrane permeability. HSE potentiated AmB and caspofungin in C. glabrata, C. parapsilosis and C. albicans. Our results suggested that HSE may be explored as antifungal agents to control Candida infections.