抗真菌机制支持硼酸治疗念珠菌性阴道炎。

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De刚毛F,施密特M, Vu B, Essmann M,拉森B

抗真菌机制支持硼酸治疗念珠菌性阴道炎。

J Antimicrob Chemother。2009年2月,63 (2):325 - 36。doi: 10.1093 /江淮/ dkn486。Epub 2008年12月4。

PubMed ID

19059942 (在PubMed

]

文摘

背景:硼酸是一个经常被引用的治疗复发性和抗酵母阴道炎,但是数据对其抗真菌活性的程度和机制缺乏。目的:本研究的目的是利用体外方法理解硼酸的频谱和机制作为一个潜在的治疗阴道感染。方法:酵母和细菌隔离被琼脂稀释法检测来确定硼酸的内在抗菌活性。建立了微生物生理学方法照亮了硼酸对白色念珠菌的作用机制。结果:白念珠菌菌株(包括fluconazole-resistant株)在浓度可以达到抑制阴道内的;细菌。肉汤稀释麦克风之间的1563和6250 mg / L和硼酸证明抑制真菌的(也反映在公司减少(2)代);长期的文化在50000 mg / L是真菌的。几种有机酸在酵母氮肉汤了pH值低于克分子数相等的硼酸和硼酸钠,但不抑制。感冒或厌氧孵化保护酵母高硼酸浓度。 Cells maintained integrity for 6 h in boric acid at 37 degrees C, but after 24 h modest intrusion of propidium iodide occurred; loss of plate count viability preceded uptake of vital stain. Growth at sub-MIC concentrations of boric acid decreased cellular ergosterol. The drug efflux pump CDR1 did not protect Candida as CDR1 expression was abrogated by boric acid. Boric acid interfered with the development of biofilm and hyphal transformation. CONCLUSIONS: Boric acid is fungistatic to fungicidal depending on concentration and temperature. Inhibition of oxidative metabolism appears to be a key antifungal mechanism, but inhibition of virulence probably contributes to therapeutic efficacy in vivo.

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药物

硼酸

四硼酸钠