黑素瘤皮肤寡肽对紫外线b照射人角质形成细胞的保护作用

Z. Wang, Lisha Dong, Jiaojiao Han, Jun Zhou, Chenyang Lu, Ye Li, Tinghong Ming, Rixin Wang, Zhen Zhang, X. Su
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引用次数: 0

摘要

紫外线B (UVB)诱导的细胞死亡导致皮肤光老化。在这项研究中,我们研究了黑素瘤皮肤寡肽(MSOP)对uvb照射的人角质形成细胞的保护作用。优化了MSOP的制备方法,鉴定出了3个高丰度肽段VADML (Val-Ala-Asp-Met-Leu)、IARF (Ile-Ala-Arg-Phe)和SSPSF (Ser-Ser-Pro-Ser-Phe)。发现工作室预测这些肽与Keap1相互作用,并有助于抗氧化活性。因此,我们采用uvb诱导的细胞模型来探讨MSOP在体外的有益作用。msop处理组超氧化物歧化酶和谷胱甘肽过氧化物酶活性升高,丙二醛含量降低。此外,通过定量蛋白质组学分析鉴定出23个差异表达蛋白;其中,参与Keap1/Nrf2/ are信号通路的Nrf2上调和Keap1下调参与了抗氧化过程。基于这项研究,MSOP可能是一种保护皮肤免受UVB照射的替代剂。
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Protective effect of Melanogrammus aeglefinus skin oligopeptide in ultraviolet B-irradiated human keratinocytes
Ultraviolet B (UVB)-induced cell death causes skin photoaging. In this study, we investigated the protective effect of Melanogrammus aeglefinus skin oligopeptide (MSOP) in UVB-irradiated human keratinocytes. The method of preparing MSOP was optimized, and three peptides with high abundance, VADML (Val-Ala-Asp-Met-Leu), IARF (Ile-Ala-Arg-Phe) and SSPSF (Ser-Ser-Pro-Ser-Phe), were identified. Discovery Studio predicted that these peptides interacted with Keap1 and contributed to antioxidant activity. Therefore, a UVB-induced cell model was used to explore the beneficial effects of MSOP in vitro. The activities of superoxide dismutase and glutathione peroxidase were increased in the MSOP-treated groups, while the malondialdehyde content was decreased. In addition, 23 differentially expressed proteins were identified through quantitative proteomics analysis; among them, the upregulation of Nrf2 and downregulation of Keap1, which are involved in the Keap1/Nrf2/ARE signaling pathway, contributed to the antioxidant process. Based on this study, MSOP might be an alternative agent for protecting the skin against UVB exposure.
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