Phang Tze-Lee, McClellan Scott J, Franses Elias I
School of Chemical Engineering, Purdue University, 480 Stadium Mall Drive, West Lafayette, Indiana 47907-2100, USA.
Langmuir. 2005 Oct 25;21(22):10140-7. doi: 10.1021/la0504412.
Fibrinogen (FB) and other serum proteins leak into the aqueous alveolar lining layer due to lung injuries. The adsorption of these serum proteins at the air/aqueous interface can produce higher surface tensions than the pulmonary lipids, and acute respiratory distress syndrome (ARDS) can ensue. By having a molecular adsorption mechanism, as compared to a particulate adsorption mechanism of other longer chain lipids, dilauroylphosphatidylcholine (DLPC) lipid can expel FB from the air/aqueous interface at 25 degrees C, in water or in phosphate-buffered saline, as proven by tensiometry (also at 37 degrees C), ellipsometry, and infrared reflection-absorption spectroscopy. Moreover, before FB is displaced by DLPC at the interface, there is a substantial initial enhancement in the FB adsorption, consistent with some interaction or binding of DLPC with FB to produce a more hydrophobic protein surface. After the FB molecules have been displaced by DLPC, or when DLPC has already adsorbed at the interface, FB molecules are less favored to adsorb near the DLPC monolayer with the lecithin headgroups facing toward them. The results have implications for possible uses of DLPC lipid in potential lung surfactant formulations in treating patients with ARDS.
由于肺部损伤，纤维蛋白原（FB）和其他血清蛋白会渗漏到肺泡衬液层中。这些血清蛋白在气/液界面的吸附会产生比肺脂质更高的表面张力，进而可能引发急性呼吸窘迫综合征（ARDS）。与其他长链脂质的颗粒吸附机制相比，二月桂酰磷脂酰胆碱（DLPC）脂质具有分子吸附机制，通过张力测定法（37℃时也可）、椭偏仪和红外反射吸收光谱法证明，在25℃下于水或磷酸盐缓冲盐溶液中，DLPC脂质能够将FB从气/液界面驱除。此外，在界面处FB被DLPC取代之前，FB的吸附会有显著的初始增强，这与DLPC与FB之间存在某种相互作用或结合以产生更疏水的蛋白质表面一致。在FB分子被DLPC取代后，或者当DLPC已经吸附在界面时，FB分子不太倾向于吸附在卵磷脂头基朝向它们的DLPC单分子层附近。这些结果对于DLPC脂质在治疗ARDS患者的潜在肺表面活性剂制剂中的可能应用具有启示意义。
