目的研究紫外线(UV)照射对人皮肤成纤维细胞的细胞凋亡率、细胞周期变化和次黄嘌呤磷酸核糖转移酶(HPRT)基因位点突变频率的影响以及表没食子儿茶素没食子酸酯(EGCG)的干预作用。方法采用一定剂量的中、长波紫外线(UVA和UVB)慢性照射培养的新生儿包皮成纤维细胞。通过流式细胞仪检测细胞凋亡率和细胞周期变化,HPRT突变分析法检测突变频率。结果慢性UVA组引起的细胞凋亡率低于UVB组(P<0.05),而HPRT基因位点突变的频率是UVB组的4.79倍。EGCG干预组与单纯UV辐射组相比,成纤维细胞的凋亡率增加,HPRT基因位点突变的频率降低。结论慢性照射日常剂量UVA,其损伤性高于UVB。EGCG可以升高慢性UV照射引起的细胞凋亡率,降低UV照射引起的突变频率,提示EGCG可以诱导不可逆损伤细胞的凋亡,从而减少突变细胞。

ObjectiveTo observe the effect of epigallocatech in-3-gallate (EGCG) on apopto sisrate,cell cycle, hypoxan thineguanine phospho ribosyltran sferase (HPRT ) gene mutation frequency induced by long-term UVA and UVB irradiation in human skin fibrob lasts. Methods Fibrob lasts were separated from infant foreskin, and divided in to six groups, they were control, EGCG, UVA ,UVB,UVA+EGCG, and UVB+ EGCG groups. The cells were irradiated by 30 mJö cm 2UVB and 10 Jöcm 2UVA everyday for 2weeks. After irradiation, fibrob lasts were incubated with DM EM containing 10% bovine serumor the samemedium containing 25 LgömL of EGCG for 24 h. The apopto sisrate and cell cycle were detected by Flow Cytometer. The HPRT gene mutantion frequency was detected by the HPRT mutagenesis asay. ResultsUnder long-term UV irradiation, apopto sisrate and mutation frequency of fibrob lasts were increased. The apoptosisrate in long-term UVA group was lower than that in UVB group (P<0.05) ,while HPRT mutation frequency in UVA group was 4.79t imes asmuch as that in UVB group. Compared EGCG inference groups with UV groups, the apopto sisrates were increased, while HPRT gene mutation frequency was decreased.Conclusion The damage by long-term daily irradiation in UVA group is heavier than that in UVB group. The EGCG could increase the apopto sisrate of fibrob lasts induced by long-term UVirradiation and prevent the increase of themutation frequency, which indicate that the EGCG could induce the irreversible damage of apoptosis so that to reduce the mutation cells.