Walters K A, Walker M, Olejnik O
Fisons plc, Pharmaceutical Division, Loughborough, UK.
J Pharm Pharmacol. 1988 Aug;40(8):525-9. doi: 10.1111/j.2042-7158.1988.tb05295.x.
The influence of a range of polyethoxylated non-ionic surfactants upon the transport of methyl nicotinate across hairless mouse skin in-vitro was investigated using standard two-compartment diffusion cells. Those surfactants having a linear alkyl chain greater than C8 and an ethylene oxide chain length of less than E14 caused significant increases in the flux of methyl nicotinate. Surfactants having branched or aromatic moieties in the hydrophobic portion were ineffective. Maximum enhancement of flux was obtained using polyoxyethylene (10) lauryl ether (Brij 36T). Two possible modes of surfactant action are proposed. Initially the surfactant may penetrate into the intercellular regions of the stratum corneum, increase fluidity and eventually solubilise and extract lipid components. Secondly, penetration of the surfactant into the intracellular matrix followed by interaction and binding with the keratin filaments may result in a disruption of order within the corneocyte. The structural specificity required for the latter mechanism may explain, to some extent, the maximum activity obtained with the C12 surfactant.
使用标准的双室扩散池,研究了一系列聚乙氧基化非离子表面活性剂对烟酸甲酯体外透过无毛小鼠皮肤转运的影响。那些具有大于C8的直链烷基和小于E14的环氧乙烷链长度的表面活性剂会导致烟酸甲酯通量显著增加。在疏水部分具有支链或芳族部分的表面活性剂无效。使用聚氧乙烯(10)月桂基醚(Brij 36T)可获得最大通量增强。提出了两种可能的表面活性剂作用模式。最初,表面活性剂可能渗透到角质层的细胞间区域,增加流动性并最终溶解和提取脂质成分。其次,表面活性剂渗透到细胞内基质中,随后与角蛋白丝相互作用并结合,可能导致角质形成细胞内的有序结构破坏。后一种机制所需的结构特异性可能在一定程度上解释了使用C12表面活性剂获得的最大活性。