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首页> 外文期刊>Journal of dermatological science >Flavonolignans from Silybum marianum moderate UVA-induced oxidative damage to HaCaT keratinocytes.
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Flavonolignans from Silybum marianum moderate UVA-induced oxidative damage to HaCaT keratinocytes.

机译:来自水飞蓟的黄酮木聚糖对UVA诱导的HaCaT角质形成细胞的氧化损伤具有中等作用。

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BACKGROUND: UV radiation from sunlight is a very potent environmental risk factor in the pathogenesis of skin cancer. Exposure to UV light, especially the UVA part, provokes the generation of reactive oxygen species (ROS), which induce oxidative stress in exposed cells. Topical application of antioxidants is a successful strategy for protecting the skin against UV-caused oxidative damage. OBJECTIVE: In this study, silybin (SB) and 2,3-dehydrosilybin (DS) (1-50 micromol/l), flavonolignan components of Silybum marianum, were tested for their ability to moderate UVA-induced damage. METHODS: Human keratinocytes HaCaT were used as an appropriate experimental in vitro model, to monitor the effects of SB and DS on cell viability, proliferation, intracellular ATP and GSH level, ROS generation, membrane lipid peroxidation, caspase-3 activation and DNA damage. RESULTS: Application of the flavonolignans (1-50 micromol/l) led to an increase in cell viability of irradiated (20 J/cm(2)) HaCaT keratinocytes. SB and DS also suppressed intracellular ATP and GSH depletion, ROS production and peroxidation of membrane lipids. UVA-induced caspases-3 activity/activation was suppressed by treatment with SB and DS. Lower concentrations of both compounds (10 micromol/l) significantly reduced cellular DNA single strand break formation. CONCLUSION: Taken together, the results suggest that these flavonolignans suppress UVA-caused oxidative stress and may be useful in the treatment of UVA-induced skin damage.
机译:背景:来自阳光的紫外线辐射是皮肤癌发病机理中非常重要的环境风险因素。暴露于紫外线(尤其是UVA部分)会激发活性氧(ROS)的产生,从而在裸露的细胞中诱导氧化应激。局部使用抗氧化剂是保护皮肤免受紫外线引起的氧化损伤的成功策略。目的:在本研究中,对水飞蓟素的黄酮木脂素成分水飞蓟宾(SB)和2,3-脱氢水飞蓟宾(DS)(1-50 micromol / l)进行了测试,以研究其对UVA诱导的伤害的缓解能力。方法:以人角质形成细胞HaCaT作为体外实验模型,监测SB和DS对细胞活力,增殖,细胞内ATP和GSH水平,ROS生成,膜脂质过氧化,caspase-3活化和DNA损伤的影响。结果:黄酮木聚糖(1-50微摩尔/升)的应用导致辐射的(20 J / cm(2))HaCaT角质形成细胞的细胞活力增加。 SB和DS还抑制细胞内ATP和GSH的消耗,ROS的产生和膜脂质的过氧化。 UVA诱导的caspases-3活性/激活被SB和DS处理抑制。两种化合物的较低浓度(10 micromol / l)均可显着减少细胞DNA单链断裂的形成。结论:综上所述,这些结果表明这些黄酮木聚糖能抑制UVA引起的氧化应激,并可能用于治疗UVA引起的皮肤损伤。

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