摘要
目的:旨在DNA水平探讨紫外线启动人皮肤光老化的机制,以加深对光老化的理解,并为减缓光老化进程提供新靶点。方法:紫外线照射原代人成纤维细胞,用比色法测定成纤维细胞的增殖活性;用1000 mJ/cm^2紫外线照射细胞,采用实时定量PCR方法测定照射与未照射细胞不同代数的端粒长度;不同剂量紫外线照射同代细胞,并测定端粒长度。结果:紫外线照射与未照射细胞的端粒长度均有随着细胞的复制传代而逐渐缩短趋势;在不同剂量紫外线照射的同一代细胞之间,紫外线剂量越高,端粒长度则越短,高剂量组与未照射组相比有统计学差异(P<0.05)。结论:单次大剂量紫外线照射可以使端粒长度变短,急性光损伤可能启动光老化的早期进程。
Objective: To investigate the molecular mechanism of the photoaging initiated by UV irradiation. Methods: Primary cultured fibroblasts were irradiated by UV light, their proliferation was evaluated with eolorimetric assay. The cultured cells in the same passage were irradiated with different doses of UV light, while the cultured cells of different passages were irradiated with same dose of UV light. The control groups were the cells untreated with UV irradiation. The length of telomere of the cells in different groups was measured by real time PCR. Results: The length of telomere tended to be shortened through passages of cell replication in both UV-treated cells and UV-untreated cells, with much shorter in the UV-treated groups than that in the UV-untreated groups. Between the different groups at the same passage, the larger the dose of UV irradiation, the shorter the length of the telomere. The statistical difference was seen between the high irradiation-dose group and the UV-untreated group (P 〈 0.05). Conclusion: The length of telomere in the cells can be affected by a single high dose UV-irradiation and acute photodamage might initiate the early process of photoaging.
出处
《临床皮肤科杂志》
CAS
CSCD
北大核心
2009年第9期559-561,共3页
Journal of Clinical Dermatology
基金
国家自然科学基金资助项目(30872269)
关键词
光损伤
光老化
成纤维细胞
人
紫外线
端粒
photo injury
photoaging
fibroblast, human
uhraviolet light
telomere