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

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Abstract:

Background:

Ergocalciferol (VD2) 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 D3 (1α,25(OH)2D3) 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 VD2 to hairless mouse dorsal skin, and exposure to solar-simulating ultraviolet (UV) radiation at a dose of 10.8 J/cm2 (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 VD2 significantly prevented wrinkle formation and abnormal accumulation of extracellular matrix components. In addition, VD2 suppressed excessive secretion of IL-6 induced by UV irradiation in cultured human normal keratinocytes, in a dose-dependent manner. Conclusion:

VD2 promoted keratinocytes differentiation in the epidermis and showed diverse physiological effects, the same as the active form of VD3. 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 VD2 may become an effective means to suppress solar UV-induced human skin damage.

Keywords: IL-6; UV; epidermis hyperplasia; ergocalciferol; keratinocytes differentiation; photodamage

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1600-0781.2004.00116.x

Affiliations: 1: Kose Co. Research & Development Division 1-18-4 Azusawa, Itabashi-ku, Tokyo Japan, and 2: Graduate School of Pharmaceutical Sciences, Chiba University, 1-33 Yayoi, Inage, Chiba-shi, Chiba, Japan

Publication date: October 1, 2004

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