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以体外培养的不同代龄的人胚肺二倍体成纤维细胞（２ Ｂ Ｓ）为对象，紫外线诱导 Ｄ Ｎ Ａ 损伤后，观察细胞形态、增殖特性、细胞周期、 Ｄ Ｎ Ａ 修复变化等细胞应答以及 ｇａｄｄ１５３、ｐ２１ Ｗ Ａ Ｆ１／ Ｃ Ｉ Ｐ１／ Ｓ Ｄ Ｉ１、ｐ５３ 等基因的转录水平的表达变化．结果显示：紫外线诱导 Ｄ Ｎ Ａ 损伤后，衰老（＞ ５５ 代）２ Ｂ Ｓ细胞形态及增殖能力的改变不如年轻细胞（＜ ３０ 代）显著；不同代龄的细胞损伤后均出现 Ｇ１ 期阻滞现象，年轻细胞 Ｇ１ 期阻滞率明显高于衰老细胞（ Ｐ＜ ００５）；衰老细胞总的修复能力较年轻细胞明显下降（ Ｐ＜ ００１）；同时，ｇａｄｄ１５３、ｐ２１、ｐ５３ 等的可诱导性均低于年轻 ２ Ｂ Ｓ细胞．由此，分别在细胞水平与基因水平反映了衰老细胞经紫外线照射损伤后的细胞应答变化与修复机能减退的关系．
In vitro culture of human embryonic lung diploid fibroblasts (2 B S) as the object, UV-induced D N A injury, observe the cell morphology, proliferation characteristics, cell cycle, D N A repair changes and other cells Response and the expression of gadd153, p21 W A F1 / C I P1 / S D I1, p53 and other genes. The results showed that the changes of morphology and proliferation of 2 B S cells after senescence (> 55 passages) were not as remarkable as those of young cells (<30 passages) after D N A injury induced by UV light. G1 arrest occurred in different age groups (P <005). The total repair capacity of senescent cells was significantly lower than that of young cells (P <001). Meanwhile, the expression of gadd153, p21, p53, etc. Inducibility is lower than that of young 2 B S cells. Thus, at the cellular level and the gene level, respectively, the senescent cells reflect the changes of cellular response after UV irradiation and repair the relationship between hypofunction.