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Protection against UVB-induced Oxidative Stress in Human Skin Cells and Skin Models by Methionine Sulfoxide Reductase A

机译:通过甲硫氨酸亚砜还原酶A防止UVB诱导的人体皮肤细胞和皮肤模型的氧化应激

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Environmental trauma to human skin can lead to oxidative damage of proteins and affect their activity and structure. When methionine becomes oxidized to its sulfoxide form, methionine sulfoxide reductase A (MSRA) will reduce it back to methionine. We report here the increase in MSRA in normal human epidermal keratinocytes (NHEK) after ultraviolet B (UVB) radiation, as well as the reduction in hydrogen peroxide levels in NHEK pre-treated with MSRA after exposure. Further, when NHEK were pre-treated with a non-cytotoxic pentapeptide containing methionine sulfoxide, MSRA expression increased by 18.2%. Additionally, when the media of skin models were supplemented with the methionine sulfoxide pentapeptide and then exposed to UVB, a 31.1% decrease in the production of sunburn cells was measured. We conclude that MSRA contributes to the protection of proteins against UVB-induced damage and that pre-treatment with a methionine sulfoxide-containing peptide reduces oxidative damage in NHEK and skin models.
机译:对人体皮肤的环境创伤可导致蛋白质的氧化损伤,并影响其活性和结构。当甲硫氨酸被氧化成亚砜形式时,甲硫氨酸亚砜还原酶A(MSRA)将其减少回甲硫氨酸。我们在此报告在紫外线B(UVB)辐射后正常人体表皮角质形成细胞(NHEK)中MSRA的增加,以及在暴露后用MSRA预处理的NHEK中过氧化氢水平的减少。此外,当用含有甲硫氨酸亚砜的非细胞毒性戊肽预处理NHEK时,MSRA表达增加18.2%。另外,当皮肤模型的培养基补充甲硫氨酸亚砜戊肽然后暴露于UVB时,测量晒伤细胞的产生31.1%的降低。我们得出结论,MSRA有助于保护蛋白质免受UVB诱导的损伤,并且用含甲硫氨酸亚砜的肽预处理降低了NHEK和皮肤模型的氧化损伤。

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