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离子辐射通过caspase途径而非p53途径诱导Jurkat细胞凋亡
作者:刘家浩 唐洪丽 阮为勇 王伟 唐月华 
单位:东南大学附属中大医院儿科,江苏,南京,210009
关键词:半胱氨酸天冬氨酸蛋白酶 基因 p53 细胞凋亡/辐射效应 Jurkat细胞 RNA 信使 
分类号:R-33, Q345.2, R733.705
出版年·卷·期(页码):2005·24·第四期(213-217)
摘要:

目的:研究离子辐射诱导Jurkat细胞凋亡的动态趋势及其机制.方法:分别以5、10、20Gy的辐射量照射Jurkat细胞,其中一份样本在照射前加入zVAD.fmk,在照射后培养6、12、24、36和48 h收获细胞,应用AnV/PI双染和呈现sub-G1峰技术,在流式细胞仪上定量测定凋亡细胞.采用Western Blot技术检测p53蛋白的表达.结果:细胞受照射后,凋亡细胞数随培养时间的延长和辐射量的加大而增加.在6 h,只有20Gy才诱导细胞显著凋亡(P<0.005),5Gy的照射要到24h才出现明显的凋亡(P<0.05).在48h,20Gy照射诱导的凋亡细胞数是所有时间点和剂量强度中最高的(P<0.001).加有zVAD.fmk的细胞,尽管都是10Gy照射,比未加zVAD.fmk的细胞表现出凋亡细胞明显减少(P<0.005),但与未加zVAD.fmk、照射量是5Gy的细胞相比,凋亡细胞数仍显著增加(P<0.005).Jurkat细胞在照射前后都没有p53表达.结论:离子辐射诱导细胞凋亡呈现出时间和剂量效应关系;capase抑制剂zVAD.fmk部分抑制离子辐射诱导细胞凋亡;离子辐射诱导细胞凋亡的机制独立于肿瘤抑制基因p53,caspase可能在其中起重要作用.

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