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麦角钙化醇可促进无毛小鼠体内角质形成细胞的分化,并减少紫外线照射引起的光损伤。

Ergocalciferol promotes in vivo differentiation of keratinocytes and reduces photodamage caused by ultraviolet irradiation in hairless mice.

作者信息

Mitani Hiroaki, Naru Eiji, Yamashita Mika, Arakane Kumi, Suzuki Tadashi, Imanari Toshio

机构信息

Kose Co. Research & Development Division, 1-18-4 Azusawa, Itabashi-ku, Tokyo, Japan.

出版信息

Photodermatol Photoimmunol Photomed. 2004 Oct;20(5):215-23. doi: 10.1111/j.1600-0781.2004.00116.x.

Abstract

BACKGROUND

Ergocalciferol (VD(2)) is usually administered orally and it is metabolized to produce its biologically active metabolites in the liver and kidney. Active vitamin D is a well-known potent regulator of cell growth and differentiation.

PURPOSE

Active vitamin D such as 1,25-dihydroxyvitamin D(3) (1alpha,25(OH)(2)D(3)) prevents photodamage, including wrinkles and morphologic alterations. However, its clinical and cosmetic use is limited because of its potent, associated effect on calcium metabolism. We examined the efficacy of vitamin D analogues with few adverse effects for preventing skin photodamage.

METHOD

Topical application of VD(2) to hairless mouse dorsal skin, and exposure to solar-simulating ultraviolet (UV) radiation at a dose of 10.8 J/cm(2) (UVA) were performed for 15 weeks, five times a week on weekdays. At the end of the final irradiation, histological and analytical studies were performed.

RESULTS

Topical application of VD(2) significantly prevented wrinkle formation and abnormal accumulation of extracellular matrix components. In addition, VD(2) suppressed excessive secretion of IL-6 induced by UV irradiation in cultured human normal keratinocytes, in a dose-dependent manner.

CONCLUSION

VD(2) promoted keratinocytes differentiation in the epidermis and showed diverse physiological effects, the same as the active form of VD(3). The results suggested that the suppression of skin photodamage involved the promotion of keratinocytes differentiation and suppression of IL-6 secretion induced by exposure to UV. Topical application of VD(2) may become an effective means to suppress solar UV-induced human skin damage.

摘要

背景

麦角钙化醇(VD(2))通常经口服给药,在肝脏和肾脏中代谢产生其生物活性代谢产物。活性维生素D是一种众所周知的细胞生长和分化的强效调节剂。

目的

活性维生素D,如1,25-二羟基维生素D(3)(1α,25(OH)2D(3))可预防光损伤,包括皱纹和形态学改变。然而,由于其对钙代谢的强效相关作用,其临床和美容用途受到限制。我们研究了副作用较少的维生素D类似物预防皮肤光损伤的疗效。

方法

将VD(2)局部应用于无毛小鼠背部皮肤,并以10.8 J/cm(2)(UVA)的剂量暴露于模拟太阳紫外线(UV)辐射下,持续15周,工作日每周5次。在最后一次照射结束时,进行组织学和分析研究。

结果

局部应用VD(2)可显著预防皱纹形成和细胞外基质成分的异常积累。此外,VD(2)以剂量依赖性方式抑制培养的人正常角质形成细胞中紫外线照射诱导的IL-6过度分泌。

结论

VD(2)促进表皮角质形成细胞分化,并表现出与VD(3)活性形式相同的多种生理效应。结果表明,抑制皮肤光损伤涉及促进角质形成细胞分化和抑制紫外线暴露诱导的IL-6分泌。局部应用VD(2)可能成为抑制太阳紫外线诱导的人类皮肤损伤的有效手段。

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