Zhou Bing-Rong, Luo Dan, Wei Fang-Di, Chen Xiao-E, Gao Jie
Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Arch Dermatol Res. 2008 Jul;300(6):331-4. doi: 10.1007/s00403-008-0851-4. Epub 2008 Apr 10.
Exposure to ultraviolet B (UVB) irradiation is a major risk factor for the development of skin cancer. Therefore, it is important to identify agents that can offer protection against UVB-caused DNA damage. Photocarcinogenesis is caused largely by mutations at the sites of incorrectly repaired DNA photoproducts, of which the most common are the cyclobutane pyrimidine dimers (CPDs). In this study, a DNA damage model of UVB irradiation-induced fibroblasts was established. The immunocytochemical staining, immuno dot blotting and Western blotting were employed in the study. We demonstrated that pre-treatment of fibroblasts with Baicalin dose-dependently reduced the amount of UVB-generated CPDs. Compared with UVB irradiated cells, UVB-induced p53 accumulation was less pronounced in Baicalin-treated cells. Taken together, these results suggest that Baicalin prevent CPDs formation induced by UVB. Baicalin is therefore a promising protective substance against UVB radiation.
暴露于紫外线B（UVB）辐射是皮肤癌发生的主要危险因素。因此，识别能够提供针对UVB诱导的DNA损伤保护作用的物质非常重要。光致癌作用很大程度上是由DNA光产物修复错误位点的突变引起的，其中最常见的是环丁烷嘧啶二聚体（CPD）。在本研究中，建立了UVB辐射诱导的成纤维细胞DNA损伤模型。该研究采用了免疫细胞化学染色、免疫斑点印迹和蛋白质印迹法。我们证明，用黄芩苷预处理成纤维细胞可剂量依赖性地减少UVB产生的CPD数量。与UVB照射的细胞相比，UVB诱导的p53积累在黄芩苷处理的细胞中不太明显。综上所述，这些结果表明黄芩苷可预防UVB诱导的CPD形成。因此，黄芩苷是一种有前景的抗UVB辐射保护物质。
