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Growth of candida albicans biofilm is inhibited by salvia miltiorrhiza [단삼에 의한 Candida albicans 바이오필름 발달의 억제]

Authors
Lee, H.-S.Kim, Y.
Issue Date
2019
Publisher
Korean Society for Microbiology and Biotechnology
Keywords
Antifungal; Biofilm; Candida albicans; Hypha-specific gene; Salvia miltiorrhiza
Citation
Microbiology and Biotechnology Letters, v.47, no.3, pp.465 - 472
Indexed
SCOPUS
KCI
Journal Title
Microbiology and Biotechnology Letters
Volume
47
Number
3
Start Page
465
End Page
472
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/70771
DOI
10.4014/mbl.1901.01007
ISSN
1598-642X
Abstract
Candida albicans is an opportunistic human pathogen that causes infections. Candidiasis is often related to antifungal resistance because the pathogen has the ability to form biofilms. In a previous study, we found that the Salvia miltiorriza ethanol extract demonstrated anticandidal activity by altering membrane permeability and inhibiting the cell wall synthesis in C. albicans. Our results here demonstrate that 78 µg/ ml of the S. miltiorriza extract significantly diminished the early stage biofilms formed by 10 clinical C. albicans isolates by 51.3%; this was analyzed by 2,3-Bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide salt (XTT) reduction assay. The effect of the S. miltiorrhiza extract on the adhesion of C. albicans cells to polystyrene plates and germ tube formation was examined via microscopic investigation. Although the density of the adhered cells was remarkably reduced up on incubation with 39 µg/ml S. miltiorrhiza extract, germ tube formation by C. albicans was rarely affected. Quantitative real-time PCR analysis showed that the S. miltiorrhiza extract downregulated the expression of C. albicans hypha-specific genes, EAP1 by 34.7% (p < 0.001), ALS1 by 45.0% (p < 0.001), ALS3 by 48.1% (p < 0.001), and ECE1 by 21.3% (p = 0.006), respectively. Our data suggest that the S. miltiorrhiza ethanol extract significantly inhibited the early stage of biofilm formation by C. albicans by interfering with cell adhesion, by downregulating EAP1, ALS1 and ALS3, and presumably by modifying the cell wall and membrane structure. © 2019, The Korean Society for Microbiology and Biotechnology
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