Svobodová Alena, Zdarilová Adéla, Malisková Jana, Mikulková Hana, Walterová Daniela, Vostalová Jitka
Department of Medical Chemistry and Biochemistry, Faculty of Medicine and Dentistry, Palacký University, Hnevotínská 3, 775 15 Olomouc, Czech Republic.
J Dermatol Sci. 2007 Apr;46(1):21-30. doi: 10.1016/j.jdermsci.2006.12.009. Epub 2007 Feb 7.
UV radiation from sunlight is a potent environmental risk factor in skin cancer pathogenesis. UVA is the major portion of UV light reaching the earth surface ( approximately 95%) and it is reported to lead to benign and malignant tumor formation. UVA-mediated cellular damage occurs primarily through the release of reactive oxygen species (ROS) and it is responsible for inflammation, immunosuppression, photoaging and photocarcinogenesis.
The aim of our study was to investigate the potency of silymarin, the polyphenol fraction from the seeds of Silybum marianum, to modulate UVA-induced oxidative damage to human keratinocytes.
Skin epidermal cell line HaCaT, extensively used for studying the influence of UV radiation, was chosen as an experimental model. Silymarin's effect on UVA-disrupted cell viability, proliferation, mitochondrial function, and intracellular ATP and GSH level was measured. Furthermore, silymarin's potency to reduce UVA-induced ROS generation, membrane lipid peroxidation, caspase-3 activation and DNA damage was monitored.
Treatment of irradiated HaCaT (20 J/cm(2)) with silymarin (0.7-34 mg/l; 4h) resulted in concentration-dependent diminution of UVA-caused oxidative stress on all studied parameters. Silymarin application extensively reduced GSH depletion and ROS production as well as lipid peroxidation in irradiated cells. Formation of UVA-induced DNA single strand breaks and caspase-3 activity was also significantly decreased by silymarin.
The results suggest that silymarin may be beneficial in the treatment of UVA-induced skin oxidative injury and inflammation. However, further studies especially whose using human systems are needed to determine efficacy of silymarin in vivo.
阳光中的紫外线辐射是皮肤癌发病机制中的一个强大环境风险因素。紫外线A（UVA）是到达地球表面的紫外线的主要部分（约95%），据报道它会导致良性和恶性肿瘤的形成。UVA介导的细胞损伤主要通过活性氧（ROS）的释放发生，它与炎症、免疫抑制、光老化和光致癌作用有关。
我们研究的目的是调查水飞蓟宾（来自水飞蓟种子的多酚部分）调节UVA诱导的对人角质形成细胞氧化损伤的效力。
选择广泛用于研究紫外线辐射影响的皮肤表皮细胞系HaCaT作为实验模型。测量了水飞蓟宾对UVA破坏的细胞活力、增殖、线粒体功能以及细胞内ATP和谷胱甘肽（GSH）水平的影响。此外，监测了水飞蓟宾减少UVA诱导的ROS生成、膜脂质过氧化、半胱天冬酶-3激活和DNA损伤的效力。
用水飞蓟宾（0.7 - 34 mg/l；4小时）处理受辐照的HaCaT（20 J/cm²）导致在所有研究参数上UVA引起的氧化应激呈浓度依赖性降低。水飞蓟宾的应用广泛减少了辐照细胞中GSH的消耗、ROS的产生以及脂质过氧化。水飞蓟宾还显著降低了UVA诱导的DNA单链断裂的形成和半胱天冬酶-3的活性。
结果表明水飞蓟宾可能有益于治疗UVA诱导的皮肤氧化损伤和炎症。然而，需要进一步的研究，特别是使用人体系统的研究，以确定水飞蓟宾在体内的疗效。
