表没食子儿茶素-3-没食子酸酯可降低紫外线A诱导的人皮肤成纤维细胞中的次黄嘌呤磷酸核糖转移酶突变，同时衰老和凋亡率增加。
Epigallocatechin-3-gallate decreases UVA-induced HPRT mutations in human skin fibroblasts accompanied by increased rates of senescence and apoptosis.
作者信息
Xu Yang, Zhu Jie, Zhou Bingrong, Luo Dan
机构信息
Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University;
出版信息
Exp Ther Med. 2012 Apr;3(4):625-630. doi: 10.3892/etm.2012.466. Epub 2012 Jan 31.
Our study was designed to determine the protective effect of epigallocatechin-3-gallate (EGCG) on cultured human skin fibroblasts (HSFs) from multiple ultraviolet A (UVA) irradiation-induced hypoxanthine-guanine phosphoribosyl transferase (HPRT) mutant colony formation and its underlying mechanisms. In our study, the mutation frequency of the HPRT gene was examined by mutagenesis assay. Cell senescence was determined by histochemical staining of senescence-associated β-galactosidase. The apoptosis rate was detected by flow cytometry. EGCG decreased the UVA-induced HPRT gene mutation frequency by 47.85%. However, EGCG further increased the number of senescent cells by 38.92% and the apoptosis rate by 56.92% in HSFs. The photo-protective effect of EGCG on multiple UVA-exposed HSFs is related to a significant reduction in UVA-induced HPRT mutant cells. This may be caused by the induction of damaged cells to proceed to senescence and apoptosis.
我们的研究旨在确定表没食子儿茶素-3-没食子酸酯（EGCG）对多次紫外线A（UVA）照射诱导的人皮肤成纤维细胞（HSFs）次黄嘌呤-鸟嘌呤磷酸核糖转移酶（HPRT）突变集落形成的保护作用及其潜在机制。在我们的研究中，通过诱变试验检测HPRT基因的突变频率。通过衰老相关β-半乳糖苷酶的组织化学染色来确定细胞衰老。通过流式细胞术检测凋亡率。EGCG使UVA诱导的HPRT基因突变频率降低了47.85%。然而，EGCG使HSFs中的衰老细胞数量进一步增加了38.92%，凋亡率增加了56.92%。EGCG对多次UVA照射的HSFs的光保护作用与UVA诱导的HPRT突变细胞显著减少有关。这可能是由诱导受损细胞进入衰老和凋亡所致。
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