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首页> 外文期刊>Biochimica et Biophysica Acta. Molecular and cell biology of Lipids >Pulmonary surfactant function is abolished by an elevated proportion of cholesterol
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Pulmonary surfactant function is abolished by an elevated proportion of cholesterol

机译：胆固醇比例升高取消了肺表面活性剂功能

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A molecular film of pulmonary surfactant strongly reduces the surface tension of the lung epithelium-air interface. Human pulmonary surfactant contains 5-10% cholesterol by mass, among other lipids and surfactant specific proteins. An elevated proportion of cholesterol is found in surfactant, recovered from acutely injured lungs (ALI). The functional role of cholesterol in pulmonary surfactant has remained controversial. Cholesterol is excluded from most pulmonary surfactant replacement formulations, used clinically to treat conditions of surfactant deficiency. This is because cholesterol has been shown in vitro to impair the surface activity of surfactant even at a physiological level. In the current study, the functional role of cholesterol has been re-evaluated using an improved method of evaluating surface activity in vitro, the captive bubble surfactometer (CBS). Cholesterol was added to one of the clinically used therapeutic surfactants, BLES, a bovine lipid extract surfactant, and the surface activity evaluated, including the adsorption rate of the substance to the air-water interface, its ability to produce a surface tension close to zero and the area compression needed to obtain that low surface tension. No differences in the surface activity were found for BLES samples containing either none, 5 or 10% cholesterol by mass with respect to the minimal surface tension. Our findings therefore suggest that the earlier-described deleterious effects of physiological amounts of cholesterol are related to the experimental methodology. However, at 20%, cholesterol effectively abolished surfactant function and a surface tension below 15 mN/m was not obtained. Inhibition of surface activity by cholesterol may therefore partially or fully explain the impaired lung function in the case of ALI. We discuss a molecular mechanism that could explain why cholesterol does not prevent low surface tension of surfactant films at physiological levels but abolishes surfactant function at higher levels. (c) 2005 Elsevier B.V. All rights reserved.
机译：肺表面活性剂分子膜可大大降低肺上皮-空气界面的表面张力。人肺表面活性剂除其他脂质和表面活性剂特异性蛋白外，还包含5-10％的胆固醇。在表面活性剂中发现胆固醇含量升高，可从急性受伤的肺（ALI）中回收。胆固醇在肺表面活性剂中的功能作用仍存在争议。胆固醇从大多数肺表面活性剂替代制剂中排除，临床上用于治疗表面活性剂缺乏症。这是因为已经证明胆固醇在体外甚至在生理水平上也会损害表面活性剂的表面活性。在当前的研究中，胆固醇的功能作用已使用一种改进的体外表面活性评估方法，即俘获气泡表面测量仪（CBS）进行了重新评估。将胆固醇添加到一种临床使用的治疗性表面活性剂BLES（一种牛脂质提取物表面活性剂）中，并评估了表面活性，包括该物质在空气-水界面上的吸附率，其产生接近零的表面张力的能力以及获得低表面张力所需的面积压缩。相对于最小表面张力，对于不含质量分数为5％或10％的胆固醇的BLES样品，未发现表面活性的差异。因此，我们的发现表明，较早描述的生理量的胆固醇的有害作用与实验方法有关。但是，胆固醇含量为20％时，其表面活性剂功能被有效消除，并且未获得低于15 mN / m的表面张力。因此，在ALI的情况下，胆固醇对表面活性的抑制可能部分或完全解释了肺功能受损。我们讨论了一种分子机理，可以解释为什么胆固醇不能在生理水平上阻止表面活性剂膜的低表面张力，却在较高水平上消除表面活性剂的功能。 （c）2005 Elsevier B.V.保留所有权利。

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