电离辐射1次和2次照射后大鼠脑内NF κ B活性和靶基因表达。

U Raju, G J Gumin, P J Tofilon
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引用次数: 36

摘要

放疗后中枢神经系统损伤可能与诱导基因表达和细胞因子产生有关。我们之前的研究表明,大鼠星形胶质细胞原代培养物的辐照会导致NF kappa B的活化,为了确定这种效应是否也会在体内发生,我们分析了全身辐照后大鼠大脑皮层的NF kappa B活性。单次剂量15 Gy后,NF κ B活性在照射后2小时增加,8小时后恢复到未照射水平。这种增加是剂量依赖性的,从2gy开始,持续到至少22.5 Gy。辐照后皮层内NF κ B活性不伴有I κ B α的降解。在15 Gy前24 h给药7.5 Gy时,15 Gy后增加的NF κ B活性明显降低。这些结果表明,最初的辐射暴露在大脑中诱导了一个不应期,在此期间,NF κ B对后续辐射激活的易感性显著降低。对于NF κ b调节的细胞因子IL-1 β、IL-6和TNF α的诱导,这段时间对辐射的敏感性降低也很明显。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
NF kappa B activity and target gene expression in the rat brain after one and two exposures to ionizing radiation.

The central nervous system injury that can result after radiotherapy has been suggested to involve induced gene expression and cytokine production. We have previously shown that irradiation of primary cultures of rat astrocytes results in the activation of NF kappa B. To determine whether such an effect also occurs in vivo, NF kappa B activity was analyzed in the cerebral cortex of the rat brain after whole body irradiation. After a single dose of 15 Gy, NF kappa B activity was increased by 2 h postirradiation, returning to unirradiated levels by 8 hours. The increase was dose-dependent beginning at 2 Gy and continuing to at least 22.5 Gy. NF kappa B activity in the irradiated cortex was not accompanied by I kappa B alpha degradation. When 7.5 Gy was delivered 24 h before the 15 Gy, the increase in NF kappa B activity after 15 Gy was significantly reduced. These results suggest that an initial exposure to radiation induced a refractory period in the brain during which the susceptibility of NF kappa B to activation by subsequent irradiation was significantly reduced. This period of reduced sensitivity to radiation was also apparent for the induction of the NF kappa B-regulated cytokines IL-1 beta, IL-6, and TNF alpha.

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