钙三醇和氯倍他醇-17-丙酸对uvb照射下人体皮肤的影响:免疫组织化学研究。

C J van der Vleuten, C G Snijders, E M de Jong, P C van de Kerkhof
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引用次数: 13

摘要

皮质类固醇和维生素D3类似物在体外系统中抑制增殖,增强正常角化和干扰皮肤炎症。这两种治疗方法对牛皮癣都有效,尽管一些报告表明,维生素D3在减少炎症变化方面的效果不如其对角质细胞生长和分化的有效作用。本研究的目的是比较和对比维生素D3类似物钙化三醇、氯倍他醇-17-丙酸和安慰剂对正常人类皮肤中标准化紫外线B (UVB)辐射单次刺激引起的表皮生长、角化和炎症的免疫组织化学标志物的影响。氯倍他索对uvb诱导的表皮细胞增殖、tenascin诱导、角蛋白16诱导以及T淋巴细胞和cd1a阳性细胞的聚集具有抑制作用。氯倍他索引起的表皮变薄也被观察到。氯倍他索对UVB刺激后的终末分化没有增强作用。相比之下,在UVB刺激后,钙三醇减少了转谷氨酰胺酶阳性细胞的成员,但增加了表皮的厚度,但对角化、表皮增殖和炎症的其他标志物没有显著影响。目前的研究再次证实了局部皮质类固醇对uvb挑战皮肤的各个方面的有效作用。相比之下,钙化三醇尤其干扰了一条分化途径(谷氨酰胺转氨酶),而没有调节其他uvb诱导的变化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of calcipotriol and clobetasol-17-propionate on UVB-irradiated human skin: an immunohistochemical study.

Corticosteroids and vitamin D3 analogues inhibit proliferation, enhance normal keratinisation and interfere with cutaneous inflammation in in vitro systems. Both treatments are effective in psoriasis, although several reports suggest that vitamin D3 is less effective in reducing the inflammatory changes compared to its potent effect on keratinocyte growth and differentiation. The aim of the present study was to compare and contrast the effects of the vitamin D3 analogue calcipotriol, clobetasol-17-propionate and a placebo on immunohistochemical markers for epidermal growth, keratinisation and inflammation induced by a standardised single challenge with ultraviolet B (UVB) radiation in normal human skin. Clobetasol proved to inhibit UVB-induced proliferation of epidermal cells, tenascin induction, keratin 16 induction and the accumulation of T lymphocytes and CD1a-positive cells. Epidermal thinning due to clobetasol was also observed. No effect of clobetasol was shown on the enhanced terminal differentiation following UVB challenge. In contrast, calcipotriol reduced the member of transglutaminase-positive cells following UVB challenge but increased the thickness of the epidermis without a significant effect on other markers for keratinisation, epidermal proliferation and inflammation. The present study reconfirms the potent effect of topical corticosteroids on various aspects of UVB-challenged skin. In contrast, calcipotriol interfered especially with one differentiation pathway (transglutaminase) without modulation of other UVB-induced changes.

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