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实验性诱导粉刺的电子显微镜研究及维甲酸对粉刺形成的影响。

An electron microscopic study of experimentally-induced comedo and effects of vitamin A acid on comedo formation.

作者信息

Maeda T

机构信息

Department of Dermatology, Toyama Medical and Pharmaceutical University, Japan.

出版信息

J Dermatol. 1991 Jul;18(7):397-407. doi: 10.1111/j.1346-8138.1991.tb03105.x.

DOI:10.1111/j.1346-8138.1991.tb03105.x
PMID:1724252
Abstract

The mechanisms of comedogenesis and comedolysis were investigated at the ultrastructural level after applying oleic acid (OA) only, or oleic acid together with vitamin A acid (VAA), to rabbit ears daily for two weeks. 1) In the follicular epithelium of the experimentally-induced comedo (EIC) by OA, several ultrastructural changes similar to those in human comedo were observed. EIC in rabbit ears appeared to be induced both by the hyperkeratinization of the follicular epithelium and by the delayed desquamation of horny cells due to the persistence of intercellular binding apparatus. 2) VAA strongly inhibited the formation of EIC. In the follicular epithelium, two different types of changes, non-cohesive hyperkeratinization and inhibition of keratinization, were observed. These represent the cell injury and recovery stages, respectively. VAA induced the disturbance of follicular epithelial keratinization and reduction of intercellular bindings between horny cells. These effects might prevent the cohesion and accumulation of horny cells and inhibit EIC formation. 3) The number of Odland bodies (Ods) showed an inverse correlation with the cohesion of horny layer. These findings support the theory that Ods have a desquamating function as extracellular lysosomes. The change in Ods would also contribute to both EIC formation by OA and the inhibition by VAA. In addition, VAA caused a characteristic increase in Ods with lamellar structures. It is suggested that Ods with lamellar structures have a desquamating function.

摘要

在连续两周每天仅给兔耳涂抹油酸(OA)或同时涂抹油酸与维甲酸(VAA)后,在超微结构水平研究了粉刺形成和粉刺溶解的机制。1)在由OA诱导的实验性粉刺(EIC)的毛囊上皮中,观察到了一些与人类粉刺中相似的超微结构变化。兔耳中的EIC似乎是由毛囊上皮的过度角化以及由于细胞间连接装置持续存在导致角质形成细胞脱屑延迟所引起的。2)VAA强烈抑制EIC的形成。在毛囊上皮中,观察到了两种不同类型的变化,即非粘性过度角化和角化抑制,它们分别代表细胞损伤和恢复阶段。VAA诱导毛囊上皮角化紊乱以及角质形成细胞之间细胞间连接减少。这些作用可能会阻止角质形成细胞的凝聚和积累,并抑制EIC的形成。3)奥德兰小体(Ods)的数量与角质层的凝聚呈负相关。这些发现支持了Ods作为细胞外溶酶体具有脱屑功能的理论。Ods的变化也会对OA诱导的EIC形成以及VAA的抑制作用产生影响。此外,VAA导致具有层状结构的Ods显著增加。提示具有层状结构的Ods具有脱屑功能。

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