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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Resveratrol protects human keratinocytes HaCaT cells from UVA-induced oxidative stress damage by downregulating Keap1 expression.
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Resveratrol protects human keratinocytes HaCaT cells from UVA-induced oxidative stress damage by downregulating Keap1 expression.

机译：白藜芦醇通过下调Keap1表达，保护人角质形成细胞HaCaT细胞免受UVA诱导的氧化应激损伤。

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摘要

Ultraviolet radiation A (UVA)-induced oxidative stress is recognized as an important factor in the development of skin carcinogenesis. Resveratrol is demonstrated to possess remarkable antioxidant activity in the organism. The aim of this study was to investigate the protective role of resveratrol in human keratinocytes (HaCaT) against UVA-induced oxidative damage and the possible mechanism of the translocation of NF-E2-related factor-2 (Nrf2) into the nucleus. The HaCaT cells were UVA-irradiated and the effects of resveratrol on cell viability, reactive oxygen species generation and membrane-lipid peroxidation were measured. The proteins and mRNA of Nrf2 and Kelch-like-ECH-associated protein 1 (Keap1) were determined by immunofluorescence staining, Western blot and quantitative PCR, respectively. UVA exposure led to a decrease in viability and an increase in reactive oxygen species generation in HaCaT cells. Resveratrol could effectively increase the viability of HaCaT cells after UVA exposure and protect them from UVA-induced oxidative stress. Moreover, resveratrol increased the level of Nrf2 protein and facilitated Nrf2 accumulation in the nucleus; as a result, the activity of antioxidant enzymes was also upregulated. The main finding was that Keap1 protein, a repressor of Nrf2 in the cytoplasm, was clearly decreased by resveratrol treatment 12h and beyond though the level of Keap1 mRNA still increased. Our results suggest that resveratrol can degrade Keap1 protein and facilitate Nrf2 accumulation in the nucleus, thereby protecting HaCaT cells from UVA-induced oxidative stress. Resveratrol could be a more useful natural medicine for the protection of epidermal cells from UVA-induced damage.
机译：紫外线A（UVA）诱导的氧化应激被认为是皮肤致癌作用发展的重要因素。白藜芦醇被证明在生物体中具有显着的抗氧化活性。这项研究的目的是研究白藜芦醇在人角质形成细胞（HaCaT）中对UVA诱导的氧化损伤的保护作用以及NF-E2相关因子2（Nrf2）转运入细胞核的可能机制。 HaCaT细胞经过UVA照射，并测定了白藜芦醇对细胞活力，活性氧生成和膜脂过氧化的影响。通过免疫荧光染色，Western印迹和定量PCR分别测定Nrf2和与Kelch样-ECH相关的蛋白1（Keap1）的蛋白和mRNA。 UVA暴露导致HaCaT细胞活力降低和活性氧生成增加。白藜芦醇可以有效地增加HaCaT细胞在UVA暴露后的活力，并保护它们免受UVA诱导的氧化应激。此外，白藜芦醇增加了Nrf2蛋白的水平，并促进了Nrf2在细胞核中的积累。结果，抗氧化酶的活性也被上调。主要发现是，白藜芦醇处理12h后，Keap1蛋白（一种在细胞质中抑制Nrf2的蛋白）明显降低，尽管Keap1 mRNA的水平仍在增加。我们的结果表明，白藜芦醇可以降解Keap1蛋白并促进Nrf2在细胞核中的积累，从而保护HaCaT细胞免受UVA诱导的氧化应激。白藜芦醇可能是一种更有用的天然药物，可保护表皮细胞免受UVA诱导的伤害。

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