【摘 要】
：
以HeLa细胞为实验材料,探讨了NADPH氧化酶在X射线诱导细胞损伤过程中的作用。结果显示,12Gy X射线辐照后细胞内活性氧(ROS)明显增加,在用NADPH氧化酶抑制剂处理后再辐照,则细
【机 构】
：
兰州大学临床医学院,中国科学院近代物理研究所,甘肃省人民医院,兰州大学生命科学学院,甘肃省肿瘤医院,兰州军区总医院,
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以HeLa细胞为实验材料,探讨了NADPH氧化酶在X射线诱导细胞损伤过程中的作用。结果显示,12Gy X射线辐照后细胞内活性氧(ROS)明显增加,在用NADPH氧化酶抑制剂处理后再辐照,则细胞内ROS降低到未辐照水平;同时辐照后NADPH氧化酶细胞质亚基p47phox在细胞质积聚并和细胞膜亚基gp91phox结合;Western blotting检测结果显示,NADPH氧化酶的关键亚基gp91phox的表达量明显增加。以上结果说明,NADPH氧化酶可以被X射线激活,由其介导产生的ROS在X射线诱导HeLa细胞损伤过程中扮演重要角色。
HeLa cells were used as experimental materials to explore the role of NADPH oxidase in X-ray induced cell injury. The results showed that the intracellular reactive oxygen species (ROS) increased significantly after irradiation with 12Gy X-rays, and decreased after treatment with NADPH oxidase inhibitor, then the intracellular ROS decreased to the unirradiated level. At the same time, NADPH oxidase The cytoplasmic subunit p47phox accumulated in the cytoplasm and bound to the cell membrane subunit gp91phox. The results of Western blotting showed that the expression of gp91phox, a key subunit of NADPH oxidase, was significantly increased. The above results indicate that NADPH oxidase can be activated by X-ray and the ROS mediated by it play an important role in X-ray-induced HeLa cell injury.
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