表面活性剂诱导神经酰胺和其他细胞间脂质耗竭:导致角质层脱水的机制暗示

G. Imokawa
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引用次数: 30

摘要

为了阐明表面活性剂诱导角质层脱水的机制,我们首先通过去除完整人体角质层中的细胞间脂质和吸湿物质来检测角质层的保水性。细胞间脂质的消耗很容易导致角质层脱水,但不受额外水处理的影响,因为水处理会释放大量的吸湿物质,包括氨基酸。与此一致的是,将分离的细胞间脂质或其亚组分应用于脂质耗尽和脱水的SC,可以挽救减少的含水量以及明显的结垢,尽管甘油没有这样的效果。平行差示扫描量热分析表明,脂质消耗导致SC降低了非冷冻结合水的含量,分离的细胞间脂质的应用使结合水的含量恢复到对照水平。另一方面,从脂质耗尽的SC中额外释放的吸湿物质并不影响结合水的含量。基于上述SC中的本构持水机制,我们评估了表面活性剂诱导SC脱水的物理化学机制,从而导致紧绷感和皮肤粗糙。与丙酮/乙醚处理类似,表面活性剂处理释放大量细胞间脂质,其强度因不同表面活性剂而异,但与诱导SC脱水的强度相关,导致皮肤紧绷感和皮肤粗糙。恢复或抑制实验表明,表面活性剂处理引起的SC脱水可以通过应用分离的细胞间脂质或在洗涤过程中添加单甘油酯(MG)来显着减弱,从而显着降低皮肤粗糙度。后一项研究表明,尽管表面活性剂处理过程中皮脂成分和氨基酸的释放不受MG的影响,但神经酰胺的去除却因MG的加入而显著减弱,这表明神经酰胺的消耗在诱导表面活性剂诱导的SC脱水中起着重要作用。上述研究结果共同表明,神经酰胺在SC中的含量与SC水化的调节密切相关,表面活性剂处理导致的神经酰胺缺乏是表面活性剂诱导的SC脱水的主要原因。合成的伪神经酰胺在防止或消除SC脱水方面非常有效,这一事实进一步加强了这一假设,而SC脱水是诱导紧感和兴奋的内在因素皮肤粗糙,这为特应性皮肤干燥提供了病理基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Surfactant-Induced Depletion of Ceramides and Other Intercellular Lipids: Implication for the Mechanism Leading to Dehydration of the Stratum corneum
In order to clarify the mechanisms underlying the surfactant-induced dehydration of the stratum corneum (SC), we first examined the constitutive water-holding function of the SC by removing intercellular lipids as well as hygroscopic materials from intact human SC. The dehydration of the SC can be easily induced by depletion of intercellular lipids, but was not affected by an additional water treatment, which releases a large amount of hygroscopic materials including amino acids. Consistent with this, the application of isolated intercellular lipids or their subfractions to the lipid-depleted and dehydrated SC rescues the decreased water content as well as marked scaling, although glycerine did not have such an effect. Parallel differential scanning calorimetry analysis revealed that lipid depletion causes the SC to reduce the nonfreezable bound water content and that application of isolated intercellular lipids recovered the bound water content up to the control level. On the other hand, the additional release of hygroscopic materials from lipid-depleted SC did not affect the bound water content. Based upon the above constitutive water-holding mechanism in the SC, we assessed the physicochemical mechanisms involved in surfactant-induced dehydration of the SC, leading to tight sensation and skin roughness. Similar to treatment with acetone/ether, treatment with surfactant releases a significant amount of intercellular lipids, the intensity of which varies among various surfactants but correlates well with the intensity of the induced dehydration of the SC leading to the tight skin sensation and skin roughness. Recovery or inhibition experiments revealed that the dehydration of the SC induced by surfactant treatment is significantly attenuated by the application of isolated intercellular lipids or by the addition of monoglyceride (MG) during the washing process, which results in a significant reduction in skin roughness. The latter study showed that whereas the release of sebum components and amino acids during surfactant treatment is not affected by the addition of MG, the removal of ceramides is significantly attenuated by the addition of MG, which suggests an essential role for ceramide depletion in the induction of the surfactant-induced dehydration of the SC. In conclusion, the above findings collectively suggest that the ceramide content in the SC is strongly associated with the regulation of SC hydration and that its deficiency due to surfactant treatment is essentially responsible for the surfactant-induced dehydration of the SC. This hypothesis is further strengthened by the fact that synthetic pseudoceramides are remarkably effective in preventing or abolishing the dehydration of the SC which is an intrinsic factor for inducing the tight sensation and roughness of the skin and which provides a pathological basis for atopic dry skin.
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