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Epigallocatechin-3-gallate decreases UVA-induced HPRT mutations in human skin fibroblasts accompanied by increased rates of senescence and apoptosis

机译:Epigallocatechin-3-gallate降低UVA诱导的人皮肤成纤维细胞HPRT突变并伴随衰老和凋亡率增加

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摘要

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.
机译:我们的研究旨在确定表没食子儿茶素-3-没食子酸酯(EGCG)对多种紫外线A(UVA)辐射诱导的次黄嘌呤-鸟嘌呤磷酸核糖基转移酶(HPRT)突变菌落形成及其潜在的人皮肤成纤维细胞(HSF)的保护作用。机制。在我们的研究中,通过诱变分析检查了HPRT基因的突变频率。通过衰老相关的β-半乳糖苷酶的组织化学染色确定细胞的衰老。用流式细胞仪检测细胞凋亡率。 EGCG使UVA诱导的HPRT基因突变频率降低了47.85%。然而,EGCG进一步使HSFs中的衰老细胞增加了38.92%,凋亡率增加了56.92%。 EGCG对多种UVA暴露的HSF的光保护作用与UVA诱导的HPRT突变细胞的显着减少有关。这可能是由于诱导受损细胞进行衰老和凋亡所致。

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