Yuan Chao, Wang Xue-Min, Yang Li-Jie, Wu Pei-Lan
Department of Skin & Cosmetic Research, Shanghai Skin Disease Hospital, Shanghai, China.
Int J Dermatol. 2014 Aug;53(8):959-65. doi: 10.1111/ijd.12099. Epub 2013 Aug 22.
Tranexamic acid (TA) is a traditional plasmin inhibitor, and its role in the renovation of damaged skin has become the topic of a lot of research. The aim of this study is to determine whether TA could repair the skin barrier by means of tight intercellular junctions.
Two kinds of damaged skin models were set up and subjected to repeated application of sodium lauryl sulfate and irradiation of ultraviolet B. Through bioengineering technology and immunohistochemistry tests, TA-induced changes in skin were detected.
After 1, 3, 7, and 14 days of application, TA can significantly accelerate barrier recovery and decrease the melanin index values of ultraviolet B irritation skin. The mean optic density of occludin from TA treatment is higher than from self-repair.
These experiments suggest that TA can accelerate skin barrier recovery and upregulate occludin induced by physicochemical damages of human skin, but it is advisable to perform more research on the upregulation of occludin in molecular mechanism in the future.
氨甲环酸(TA)是一种传统的纤溶酶抑制剂,其在受损皮肤修复中的作用已成为众多研究的课题。本研究的目的是确定TA是否能通过紧密的细胞间连接来修复皮肤屏障。
建立两种受损皮肤模型,反复应用十二烷基硫酸钠并进行紫外线B照射。通过生物工程技术和免疫组织化学试验,检测TA引起的皮肤变化。
应用TA 1、3、7和14天后,TA可显著加速屏障恢复,并降低紫外线B照射皮肤的黑色素指数值。TA处理组闭合蛋白的平均光密度高于自我修复组。
这些实验表明,TA可加速皮肤屏障恢复,并上调人体皮肤物理化学损伤诱导的闭合蛋白,但未来建议对闭合蛋白上调的分子机制进行更多研究。