Inhibitory activity of hinokitiol against biofilm formation in fluconazole-resistant Candida species.
Inhibitory activity of hinokitiol against biofilm formation in fluconazole-resistant Candida species.
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DOI：
10.1371/journal.pone.0171244
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Kim SW
中科院分区：
文献类型：
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作者：
Kim DJ;Lee MW;Choi JS;Lee SG;Park JY;Kim SW
本研究的目的是研究扁柏酚抑制念珠菌生物膜形成的能力。通过用XTT测定定量生物膜代谢活性来评价生物膜抑制。扁柏酚有效地防止生物膜形成的氟康唑敏感和氟康唑耐药菌株的念珠菌。我们确定了先前与C生物膜发育有关的特定基因的表达水平。用实时荧光定量RT-PCR法检测白念珠菌细胞的表达。与粘附过程相关的基因HWP 1和ALS 3的表达水平被扁柏酚下调。负责长期菌丝维持的UME 6和HGC 1的转录水平也被扁柏酚降低。扁柏酚抑制了CYR 1的表达，CYR 1编码菌丝形成的信号通路组分-cAMP-PKA。其上游一般调节因子RAS 1也被扁柏酚抑制。这些结果表明，扁柏酚可能具有治疗和预防生物膜相关念珠菌感染的治疗潜力。
The aim of this study was to investigate the ability of hinokitiol to inhibit the formation of Candida biofilms. Biofilm inhibition was evaluated by quantification of the biofilm metabolic activity with XTT assay. Hinokitiol efficiently prevented biofilm formation in both fluconazole-susceptible and fluconazole-resistant strains of Candida species. We determined the expression levels of specific genes previously implicated in biofilm development of C. albicans cells by real-time RT-PCR. The expression levels of genes associated with adhesion process, HWP1 and ALS3, were downregulated by hinokitiol. Transcript levels of UME6 and HGC1, responsible for long-term hyphal maintenance, were also decreased by hinokitiol. The expression level of CYR1, which encodes the component of signaling pathway of hyphal formation-cAMP-PKA was suppressed by hinokitiol. Its upstream general regulator RAS1 was also suppressed by hinokitiol. These results indicate that hinokitiol may have therapeutic potential in the treatment and prevention of biofilm-associated Candida infections.