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X射线诱导转录因子活化与凋亡的关系

Relationship between X-rays-induced activation of transcription factors and apoptosis
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摘要 目的 通过观察较高剂量照射的鼠胸腺细胞内几种转录因子活性的变化和胸腺细胞凋亡发展时程 ,探讨转录因子活性的变化在辐射诱导的免疫细胞凋亡中的作用。方法 通过电泳移动变化分析及流式细胞术的方法分别检测了 2GyX射线全身照射后胸腺细胞内转录因子NF κB、CREB和OCT 1活性以及胸腺细胞凋亡的动态变化。结果  2GyX射线全身照射后胸腺细胞内NF κB两种二聚体p5 0 p5 0和p5 0 p6 5的DNA结合活性的变化存在着明显的区别 ,主要以p5 0 p5 0活性显著升高为特征 ,CREB和OCT 1的活性也明显增强 ,活性高峰均出现于照射后 4~ 12h ,而它们的活性高峰又恰与 2Gy照射诱导的胸腺细胞凋亡的高峰相吻合。结论 较高剂量电离辐射主要诱导NF κB同源二聚体的DNA结合活性增强 ;3种转录因子NF κBp5 0 p5 0、CREB以及OCT 1可能在 2Gy照射诱导的胸腺细胞内具有协同促进细胞凋亡的作用。 Objective To investigate the role of activation of transcription factors in the induction of apo- ptosis of immune cells after whole-body irradiation (WBI)with X-rays by comparing the time course of the changes of DNA-binding activity of several transcription factors and that of apoptosis in mouse thymocyte after 2 Gy X-rays. Methods The dynamic changes of the activity of transcription factors NF-κB,CREB and OCT-1,as well as thymocyte apoptosis after whole body irradiation with 2 Gy X-rays were respectively examined with electrophoresis mobility shift assay (EMSA) and flow cytomentry (FCM). Results There was a significant distinction between the changes of DNA-binding activity of two dimers of NF-κB(p50/p50 and p50/p65) in thymocytes after WBI with 2 Gy X-rays,with significant increase in the binding activity of NF-κB homodimer p50/p50.In addition,the activity of CREB and OCT-1 also increased significantly.Their activity peaks at 4-12 h after WBI coincided well with the peaking time of thymocyte apoptosis. Conclusions WBI with 2 Gy X-rays mainly induces the activation of NF-κB homodimer p50/p50.The results suggest that the three transcription factors including NF-κB p50/p50,CREB and OCT-1 might act synergistically in the induction of apoptosis in thymocytes after WBI with 2 Gy X-rays.;
出处 《中华放射医学与防护杂志》 CAS CSCD 北大核心 2002年第1期4-6,共3页 Chinese Journal of Radiological Medicine and Protection
基金 国家自然科学基金资助项目 ( 395 70 188)
关键词 X射线 胸腺细胞 细胞凋亡 转录因子 NF-ΚB CREB OCT-1 X-rays Thymocytes Apoptosis Transcription factors NF-κB CREB OCT-1
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