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目的 探讨在紫外线诱导的人晶状体上皮细胞DNA损伤修复过程中端粒酶活性和氧化损伤蛋白的变化和作用。方法 采用照射剂量为0 0(对照组)及0 .5、1. 5、2 .5、3 .5、5 .0、7 .5、10 0mJ/cm2 (实验1~7组)的紫外线照射人晶状体上皮细胞,采用端粒酶重复序列扩增酶联免疫吸附测定法检测端粒酶活性,采用免疫印迹法检测p53、DNA损伤诱导生长停顿基因(GADD45)、增殖细胞核抗原(PCNA)及细胞周期依赖激酶抑制剂p16的蛋白表达水平。结果 对照组和实验1~7组的端粒酶活性呈上调趋势, 8组比较差异有统计学意义(F=45. 65,P<0 .01 );对照组和实验1 ~7组的p53、GADD45、PCNA、p16的蛋白表达水平均呈上升趋势, 8组比较差异均有统计学意义(F=13 .015 52, 41 241 .40, 25. 084 19, 44 331 .72;P<0. 01)。结论 在紫外线诱导的人晶状体上皮细胞DNA损伤修复过程中,端粒酶活性上调,氧化损伤蛋白的表达水平上升。端粒酶活性的上调既加强了保护细胞的作用,又增强了增殖作用;氧化损伤蛋白表达水平的提高在紫外线诱导的人晶状体上皮细胞DNA损伤修复过程中发挥关键作用;端粒酶活性上调与氧化损伤蛋白表达水平提高有关。
OBJECTIVE: To investigate the changes and roles of telomerase activity and oxidative damage proteins during UV-induced DNA damage repair of human lens epithelial cells. Methods The irradiation dose of 0 0 (control group) and 0.5, 1.5, 2.5, 3.5, 5.5, 7.0, 5 and 10 mJ / cm2 Human lens epithelial cells were detected for telomerase activity by telomerase repeat amplification enzyme-linked immunosorbent assay (ELISA), p53, DNA damage-induced growth arrest gene (GADD45), proliferating cell nuclear antigen (PCNA) The cycle depends on the protein expression level of the kinase inhibitor p16. Results The telomerase activity of the control group and the experimental groups 1 to 7 showed an upward trend. The difference between the 8 groups was statistically significant (F = 45.65, P <0.01). In the control group and the experimental groups 1 to 7, p53 , GADD45, PCNA and p16 all showed an upward trend. There were significant differences among the 8 groups (F = 13.015 52, 41 241 .40, 25. 084 19, 44 331 .72; P 0 01). Conclusion In the process of UV-induced DNA damage repair of human lens epithelial cells, the telomerase activity is up-regulated and the expression of oxidative damage protein is increased. The upregulation of telomerase activity not only enhanced the function of protecting cells but also enhanced the proliferation. The increase of the expression of oxidative damage protein played a key role in the UV-induced DNA damage repair of human lens epithelial cells. The up-regulation of telomerase activity Oxidative damage protein expression levels.