Mawson Institute, University of South Australia, Adelaide, Australia.
Langmuir. 2013 Aug 13;29(32):10279-86. doi: 10.1021/la401804e. Epub 2013 Jul 31.
The ability to observe interactions of drugs with cell membranes is an important area in pharmaceutical research. However, these processes are often difficult to understand due to the dynamic nature of cell membranes. Therefore, artificial systems composed of lipids have been used to study membrane properties and their interaction with drugs. Here, lipid vesicle adsorption, rupture, and formation of planar lipid bilayers induced by various antibiotics (surfactin, azithromycin, gramicidin, melittin and ciprofloxacin) and the detergent dodecyl-b-D-thiomaltoside (DOTM) was studied using reflective interferometric Fourier transform spectroscopy (RIFTS) on an oxidized porous silicon (pSi) surface as a transducer. The pSi transducer surfaces are prepared as thin films of 3 μm thickness with pore dimensions of a few nanometers in diameter by electrochemical etching of crystalline silicon followed by passivation with a thermal oxide layer. Furthermore, the sensitivity of RIFTS was investigated using three different concentrations of surfactin. Complementary techniques including atomic force microscopy, fluorescence recovery after photobleaching, and fluorescence microscopy were used to validate the RIFTS-based method and confirm adsorption and consequent rupture of vesicles to form a phospholipid bilayer upon the addition of antibiotics. The method provides a sensitive and real-time approach to monitor the antibiotic-induced transition of lipid vesicles to phospholipid bilayers.
药物与细胞膜相互作用的观察能力是药物研究中的一个重要领域。然而,由于细胞膜的动态性质,这些过程往往难以理解。因此,人们已经使用由脂质组成的人工系统来研究膜特性及其与药物的相互作用。在这里,使用反射干涉傅里叶变换光谱(RIFTS)研究了各种抗生素(表面活性素、阿奇霉素、短杆菌肽、蜂毒素和环丙沙星)和去污剂十二烷基-β-D-硫麦芽糖苷(DOTM)在氧化多孔硅(pSi)表面作为传感器诱导的脂质囊泡吸附、破裂和平面脂质双层的形成。pSi 传感器表面通过对单晶硅进行电化学蚀刻,然后用热氧化物层进行钝化,制备成厚度为 3 μm 的薄膜,其孔径为几纳米。此外,还使用三种不同浓度的表面活性素来研究 RIFTS 的灵敏度。原子力显微镜、光漂白后荧光恢复和荧光显微镜等互补技术用于验证基于 RIFTS 的方法,并确认抗生素的加入会导致囊泡吸附和随后破裂,形成磷脂双层。该方法提供了一种灵敏且实时的方法来监测脂质囊泡向磷脂双层的抗生素诱导转变。