|国家知识仓储
首页|科研产出|中波紫外线致16HBE细胞损伤及其机制

中波紫外线致16HBE细胞损伤及其机制OA北大核心CSCDCSTPCD

Mechanisms of ultraviolet B irradiation-induced injuries in 16HBE cells

中文摘要英文摘要

目的 探讨中波紫外线(UVB)照射对人支气管上皮细胞(16HBE)的生物学效应及其机制.方法 细胞分为不同照射剂量同一观察时间组(剂量分别为0、10、30、50、70、100 J/m2,观察时间为照后12 h)和同一剂量不同观察时间组(剂量为50 J/m2,观察时间为照后2、4、8、12、24 h)以观察UVB对16HBE细胞的存活率的影响;琼脂糖凝胶电泳观察细胞接受50 J/m2照射后其DNA的断裂情况、流式细胞术检查细胞周期、Western blot检查NF-kB的表达情况.结果 UVB照射后,可使16HBE细胞的存活率下降;DNA出现明显的"梯状条带";细胞发生S期阻滞以及NF-kB蛋白的表达增强.结论 UVB照射能引起16HBE细胞生长抑制和凋亡;其作用机制可能与NF-kB蛋白的表达增强有关.

Objective To investigate the biological effects of ultraviolet B (UVB) irradiation on human bronchial epithelial cells (16HBE cells) and explore the possible mechanism. Methods The survival rates of 16HBE cells were detected by MTT assay at 12 h after UVB irradiation at different doses (0,10, 30, 50, 70, and 100 J/m2) or at 50 J/m2 for different durations (2, 4, 8,12, and 24 h). The DNA ladder was detected by agarose gel electrophoresis, the cell cycle changes were analyzed by flow cytometry, and the expression of nuclear factor-kB (NF-KB)/p65 protein was assayed by Western blotting following the exposures. Results UVB irradiation of the cells resulted in lowered cell survival rates, DNA fragmentation, S phase arrest and up-regulation of NF-icB/p65 protein expression. Conclusions UVB irradiation can induce growth inhibition and apoptosis of 16HBE cells, in which process NF-kB protein may play a key role.

吕超;丁振华;周美娟

南方医科大学公共卫生与热带医学学院放射医学系,广东,广州,510515南方医科大学公共卫生与热带医学学院放射医学系,广东,广州,510515南方医科大学公共卫生与热带医学学院放射医学系,广东,广州,510515

医药卫生

UVB16HBE细胞细胞存活率NF-kB细胞凋亡

ultraviolet B 16HBE cells cell viability nuclear factor-kB apoptosis

《南方医科大学学报》 2011 (1)

miR-365/465在UVB致细胞周期阻滞时的调控作用及其与p53信号转导网络的关系

57-60,4

国家自然科学基金(30970673)

全文链接

https://opaj.napstic.cn/periodicalArticle/downloadReview/0120111006233877

评论