本研究拟观察人胚肺二倍体成纤维细胞(2BS、WI38)DNA聚合酶δ增龄性表达变化及营养水平对其表达的影响,观察基因损伤修复增龄性变化遗传性疾病模型-DNA损伤修复缺陷性疾病及常见老年病患者淋巴细胞DNA聚合酶δ表达变化，初步分析其作为衰老及衰老相关疾病标志物的可能性，为衰老研究标准化、衰老相关疾病诊断及健康评估提供可靠指标。.利用DNA聚合酶δ真核表达载体转染技术等，通过观察细胞传代次数、衰老表型出现时间、细胞生长增殖能力、晚期糖基化终末产物水平、衰老相关β半乳糖苷酶阳性率等，分析DNA聚合酶δ对复制性衰老的影响；通过观察DNA聚合酶δ转染细胞DNA合成率、端区缩短速度、DNA损伤水平与修复能力、衰老主导基因表达水平等，分析揭示DNA聚合酶δ调控复制性衰老的分子通路及可能机制。

This study is to observe the change of DNA polymerase δ in the replicative senescence of human fetal lung diploid fibroblast(2BS,WI38),and the effect of the nutrition in culture on the expression of DNA polymerase δof the cultured cells.Moreover,the expression change of DNA polymerase δ in lymphocyte of senescence-associated diseases,including the diseases associated with the deficiency of DNA damage repair,is also to be observed to analyze initially the potential of DNA polymerase δ as the marker of senescence as well as senescence-associated diseases.This study is also to prepare for the basic work of the enzyme in the usefulness of study standardization, diagnosisof the diseases, and healthy evaluatation of individual..With the transfection of the expression vector of DNA polymerase δ,the population doubling numbers(PDs), senescent phenotype, the potential of cell proliferation,the level of advanced glycation end products (AGEs) and the positive cell rates of senescence-associated β-galactosidase (SA-β-Gal) of the cells will be observed to analyze the effect of DNA polymerase δ on replicative senescence.And,the speed of DNA formation(Brdu),the DNA damage and repair ability, the telomere shortenning rate and the expression levels of senescence-associated genes of the transfected cells will also be observed to discover the passway & molecular mechanism of its delay of replicative senescence.