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NOX家族在X射线诱导PC-3细胞损伤中的作用

韩晓燕 刘箐 高丽萍 马建秀 黄超杰 张红

癌变·畸变·突变2012,Vol.24Issue(1):30-34,38,6.
癌变·畸变·突变2012,Vol.24Issue(1):30-34,38,6.DOI:10.3969/j.issn.1004-616x.2012.01.007

NOX家族在X射线诱导PC-3细胞损伤中的作用

Role of NOX family in PC-3cell damage induced by X-ray irradiation

韩晓燕 1刘箐 2高丽萍 2马建秀 3黄超杰 1张红4

作者信息

  • 1. 兰州大学基础医学院生物化学与分子生物学研究所,兰州730000
  • 2. 中国科学院近代物理研究所重离子辐照生物医学研究中心,兰州730000
  • 3. 上海理工大学医疗器械与食品学院,上海200093
  • 4. 西北民族大学医学院机能教研室,兰州730030
  • 折叠

摘要

Abstract

OBJECTIVE: To study the role of NOX (NADPH oxidase) in X-ray-induced damage of human androgen-independent prostate cancer PC-3 cells damage, search for potential targets for radiation sensitization. METHODS: The viability of human androgen-independent prostate cancer PC-3 cells induced by 0, 1, 2, 4 and 12 Gy of X rays after 24, 48 and 96 h was detected by the MTT assay. The level of ROS after X-ray irradiation for 15, 30, 60 and 120 min , and the expression of NOX1-5 protein in PC-3 cells induced by 0, 1 and 4 Gy of X rays was analyzed by using DCFH-DA as a probe and by Western blot, respectively. RESULTS: Compared with non-irradiated, the viability of human prostate cancer PC-3 cells induced by 1, 2, 4 and 12 Gy of X rays was significantly decreased (P<0.05) . The level of ROS reached a maximum at 60 min after 1 and 4 Gy of X-ray irradiation. NOX inhibitor DPI and antioxidant NAC pretreatment could reduce the generation of ROS. Western blotting showed the expressions of NOX1, NOX2 and NOX5 were increased after irradiation. CONCLUSION: X-ray-induced the homologs NOX1, NOX2 and NOX5 of the catalytic subunit gp91phox of NADPH oxidase over-expression, resulting in excessive intracellular ROS which is a new mechanism of X-ray-induced damage of prostate cancer cells.

关键词

NOX/活性氧/人前列腺癌细胞PC-3/X射线

Key words

NADPH oxidase/ reactive oxygen species/ human prostate cancer PC-3 cells/ X-ray

分类

医药卫生

引用本文复制引用

韩晓燕,刘箐,高丽萍,马建秀,黄超杰,张红..NOX家族在X射线诱导PC-3细胞损伤中的作用[J].癌变·畸变·突变,2012,24(1):30-34,38,6.

基金项目

国家自然科学基金(30870586):973计划(2010CB83-4200) (30870586)

癌变·畸变·突变

OACSCDCSTPCD

1004-616X

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