^(60)Coγ射线对HaCaT细胞损伤的模型建立及其机制  

Model of HaCaT cell injury induced by^(60)Co γ-rays and the underlying mechanism

作　　者：黄从书 朱贵花 刘桂芳 谢光辉 马增春[1,3] 高月 HUANG Congshu;ZHU Guihua;LIU Guifang;XIE Guanghui;MAZengchun;GAO Yue(Guangdong Pharmaceutical University,Guangzhou 510006,China;Jiangxi University of Traditional Chinese Medicine,Nanchang 330004,China;Institute of Radiation Medicine,Academy of Military Medical Sciences,Academy of Military Sciences,Beijing 100850,China)

机构地区：[1]广东药科大学,广州510006 [2]江西中医药大学,南昌330004 [3]军事科学院军事医学研究院辐射医学研究所,北京100850

出　　处：《辐射研究与辐射工艺学报》2021年第4期38-44,共7页Journal of Radiation Research and Radiation Processing

基　　金：国防科技创新项目(19-163-12-ZD-18-003-02);全军后勤科研项目(BKJ18J003)资助。

摘　　要：建立放射性皮肤损伤细胞模型,考察不同吸收剂量^(60)Coγ射线对HaCaT细胞的损伤及机制。单次剂量^(60)Coγ射线对HaCaT细胞进行照射(照射源距细胞3 m,剂量率100.68 cGy/min),CCK-8法检测细胞活性,水溶性四唑盐染色法测定超氧化物歧化酶(SOD)活力,硫代巴比妥酸法测定丙二醛(MDA),流式细胞术检测细胞调亡率,Westernblot检测细胞凋亡和炎症相关蛋白。^(60)Coγ射线照射HaCaT细胞(18 Gy)24 h后,细胞形态变化明显,细胞活性降低至57.50%,MDA升高到66.28μmol/mg,SOD抑制率升高至32.12%,细胞凋亡率升高至18.05%,炎症因子表达增加。^(60)Coγ射线照射(18 Gy)后孵育24 h,建立放射性皮肤损伤的HaCaT细胞模型,细胞发生损伤的机制可能与细胞氧化损伤、凋亡及炎症反应有关。The aim of this study was to investigate the damage caused to HaCaT cells by^(60)Coγ-rays at different doses and the underlying mechanism and to establish a cell model of radiation-induced skin injury.HaCaT cells were irradiated with a single dose of^(60)Coγ-rays(the radiation source was 3 m away from the cells,and the dose rate was 100.68 cGy/min).The cell activity was detected using the CCK-8 method,the vitality of superoxide dismutase(SOD)was measured using the water soluble tetrazolium salt staining method,the malondialdehyde(MDA)level was determined using the thiobarbituric acid method,the apoptosis rate was monitored through flow cytometry,and the expression of the apoptosis-and inflammation-related proteins was detected via western blotting.After irradiation with^(60)Coγ-rays at 18 Gy for 24 h,the morphology of HaCaT cells changed significantly,cell activity decreased to 57.5%,MDA level increased to 66.28μmol/mg,inhibition rate of SOD increased to 32.12%,apoptosis rate increased to 18.05%,and expression of inflammatory factors increased.After incubation for 24 h at an absorbed dose of 18 Gy,the cellular models of radiation-induced skin injury were established.The mechanism of cell injury may be related to cell oxidative damage,apoptosis,and inflammatory reaction.

关 键 词：放射性皮肤损伤 ^(60)Co γ 射线 氧化损伤 凋亡 炎症反应 

分 类 号：R811[医药卫生—放射医学]