CAJ | 학술논문

目的：观察电离辐射引起小鼠骨髓 c-kit+细胞损伤变化。方法磁珠法分选小鼠 c-kit+细胞,生物发光法检测细胞活力,活性氧探针(DCFH-DA)检测细胞内活性氧水平,集落形成数目检测克隆形成能力,流式细胞术检测细胞增殖与凋亡,基因芯片分析细胞内信号通路变化。结果与0 Gy 组(对照组)比较,c-kit+细胞受到1 Gy 和4 Gy 照射后,细胞活力下降,克隆形成能力下降,早期凋亡和晚期凋亡细胞比例增加,细胞内活性氧水平升高；与对照组比较,c-kit+细胞受到1 Gy 照射后,处于增殖期(S/G2/M 期)细胞比例增加；4 Gy 照射后处于增殖期(S/G2/M 期)细胞比例下降；c-kit+细胞受到4Gy 照射后 Srxn1、Psmb5、Cdkn1a、Smc1b、Bcl2l1、Lrdd 等基因表达上调；Mpo、Mtf1、Chek1、Rcc1 Ebag9、Ciapin1等基因表达下调。结论电离辐射能够引起骨髓 c-kit+细胞损伤,导致一系列信号通路表达变化。
목적：관찰전리복사인기소서골수 c-kit+세포손상변화。방법자주법분선소서 c-kit+세포,생물발광법검측세포활력,활성양탐침(DCFH-DA)검측세포내활성양수평,집락형성수목검측극륭형성능력,류식세포술검측세포증식여조망,기인심편분석세포내신호통로변화。결과여0 Gy 조(대조조)비교,c-kit+세포수도1 Gy 화4 Gy 조사후,세포활력하강,극륭형성능력하강,조기조망화만기조망세포비례증가,세포내활성양수평승고；여대조조비교,c-kit+세포수도1 Gy 조사후,처우증식기(S/G2/M 기)세포비례증가；4 Gy 조사후처우증식기(S/G2/M 기)세포비례하강；c-kit+세포수도4Gy 조사후 Srxn1、Psmb5、Cdkn1a、Smc1b、Bcl2l1、Lrdd 등기인표체상조；Mpo、Mtf1、Chek1、Rcc1 Ebag9、Ciapin1등기인표체하조。결론전리복사능구인기골수 c-kit+세포손상,도치일계렬신호통로표체변화。
Objective To observe the injury effect of ionizing radiation on bone marrow derived c-kit+ cells.Methods Via-bility of c-kit+ cells was measured by bioluminescence;the level of c-kit+ cells reactive oxygen species was measured by DCFH-DA, the ability of colony-forming units was reflected by CFU-GM;proliferation and apoptosis of c-kit+ cells were measured by flow cy-tometry;the variation of pathway was detected by arrays of gene chip.Results Compared to control group(0 Gy).It had a decrease of c-kit+ cells′cell viability and the ability of colony-forming units after the cells receipt irradiation with the dose of 1 Gy and 4 Gy;and the level of cell reactive oxygen species,ratio of apoptosis cells increased.After 1 Gy irradiation exposure,the ratio of prolifera-tion(S/G2/M phase)cells increased compared to control group.However,when the c-kit+ cells were receipt 4 Gy irradiation expo-sure,the ratio of proliferation(S/G2/M phase)cells decreased.After 4 Gy irradiation exposure,the up-regulate genes contained Srxn1,Psmb5,Cdkn1a,Smc1b,Bcl2l1,Lrdd and so on;the down-regulate genes contained Mpo,Mtf1,Chek1,Rcc1 Ebag9,Ciapin1 and so on.Conclusion There was injury effect of ionizing radiation on c-kit+ cells,and it could induce variation of many pathways.