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Dietary milk sphingomyelin prevents disruption of skin barrier function in hairless mice after UV-B irradiation

机译:膳食乳鞘磷脂可防止UV-B照射后无毛小鼠皮肤屏障功能的破坏

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摘要

Exposure to ultraviolet-B (UV-B) irradiation causes skin barrier defects. Based on earlier findings that milk phospholipids containing high amounts of sphingomyelin (SM) improved the water content of the stratum corneum (SC) in normal mice, here we investigated the effects of dietary milk SM on skin barrier defects induced by a single dose of UV-B irradiation in hairless mice. Nine week old hairless mice were orally administrated SM (146 mg/kg BW/day) for a total of ten days. After seven days of SM administration, the dorsal skin was exposed to a single dose of UV-B (20 mJ/cm2). Administration of SM significantly suppressed an increase in transepidermal water loss and a decrease in SC water content induced by UV-B irradiation. SM supplementation significantly maintained covalently-bound ?-hydroxy ceramide levels and down-regulated mRNA levels of acute inflammation-associated genes, including thymic stromal lymphopoietin, interleukin-1 beta, and interleukin-6. Furthermore, significantly higher levels of loricrin and transglutaminase-3 mRNA were observed in the SM group. Our study shows for the first time that dietary SM modulates epidermal structures, and can help prevent disruption of skin barrier function after UV-B irradiation.
机译:暴露于紫外线B(UV-B)辐射会导致皮肤屏障缺陷。基于较早的发现,在正常小鼠中,含有高鞘磷脂(SM)的乳磷脂可以改善角质层(SC)的水分含量,在此我们研究了日粮乳SM对单剂量紫外线诱发的皮肤屏障缺陷的影响。 -B照射在无毛小鼠中。九周大的无毛小鼠经口服SM(146 mg / kg BW /天),共十天。 SM给药7天后,将背部皮肤暴露于单剂量的UV-B(20 mJ / cm2)。 SM的施用显着抑制了由UV-B照射引起的经表皮水分流失的增加和SC水含量的降低。 SM补充剂可显着维持急性炎症相关基因(包括胸腺基质淋巴细胞生成素,白介素-1β和白介素-6)的共价结合的α-羟基神经酰胺水平和下调的mRNA水平。此外,在SM组中观察到Loricrin和transglutaminase-3 mRNA的水平明显更高。我们的研究首次表明,饮食中的SM可以调节表皮结构,并且可以帮助防止UV-B照射后皮肤屏障功能的破坏。

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