Kemény L, Przybilla B, Gross E, Arenberger P, Ruzicka T
Department of Dermatology, University of Munich, F.R.G.
J Invest Dermatol. 1991 Dec;97(6):1028-31. doi: 10.1111/1523-1747.ep12492471.
12-hydroxyeicosatetraenoic acid (12-HETE), the main eicosanoid in skin, is assumed to have both pathophysiologic effects in inflammatory skin diseases such as psoriasis and atopic eczema and a physiologic role in the biology of cutaneous reparative processes. Because 12-HETE exerts its effects via specific high-affinity epidermal receptors, and ultraviolet-B (UV-B) is capable of modulating various cell-surface molecules, the effects of single and repeated UV-B irradiations on the 12(S)-HETE binding sites in a human epidermal cell line, SCL-II, were studied. UV-B (100-300 J/m2) induced a large decrease in 12(S)-HETE binding in a dose-dependent manner. The inhibition occurred after a latency period of 6 h, reached its maximum at 18 h and slowly declined thereafter. A single UV-B dose of 300 J/m2 or repeated irradiation with 50 J/m2 of UV-B resulted in a 70% decrease in the number of binding sites (Bmax), whereas receptor affinity remained unaffected. The modulation of epidermal 12-HETE receptors by UV-B may partly explain the therapeutic effects of UV-B, but possibly also contribute to photodamage to skin.
12-羟基二十碳四烯酸（12-HETE）是皮肤中的主要类花生酸，被认为在银屑病和特应性皮炎等炎症性皮肤病中具有病理生理作用，并且在皮肤修复过程的生物学中具有生理作用。由于12-HETE通过特定的高亲和力表皮受体发挥作用，而紫外线B（UV-B）能够调节各种细胞表面分子，因此研究了单次和重复UV-B照射对人表皮细胞系SCL-II中12(S)-HETE结合位点的影响。UV-B（100 - 300 J/m²）以剂量依赖性方式导致12(S)-HETE结合大幅下降。这种抑制在6小时的潜伏期后出现，在18小时达到最大值，此后缓慢下降。单次300 J/m²的UV-B剂量或50 J/m²的UV-B重复照射导致结合位点数量（Bmax）减少70%，而受体亲和力不受影响。UV-B对表皮12-HETE受体的调节可能部分解释了UV-B的治疗效果，但也可能导致皮肤光损伤。
