γ 射线辐照小鼠中 NF-κB、促炎介质和信号通路的分子激活。
Molecular activation of NF-kappaB, pro-inflammatory mediators, and signal pathways in gamma-irradiated mice.
机构信息
Department of Pharmacy, Pusan National University, Busan, 609-735, Korea.
出版信息
Biotechnol Lett. 2010 Mar;32(3):373-8. doi: 10.1007/s10529-009-0165-4.
The effects of gamma-irradiation on inflammatory gene expression, including NF-kappaB activation, in the kidney of C57/BL6 mice exposed to 1-9 Gy doses of (60)Co gamma-irradiation. Radiation enhanced the NF-kappaB activation and oxidative stress caused a dose-dependent disruption in the redox balance. The significance of this study is the new molecular information gained on gamma-irradiation effects through the activation of pro-inflammatory genes by NF-kappaB via the MAPK signaling pathway. Considering the exquisite sensitivity of NF-kappaB and other pro-inflammatory mediators to the redox status, we conclude that the activation of inflammatory processes by irradiation is likely initiated by increased oxidative stress.
（60）Coγ射线照射对 C57/BL6 小鼠肾脏中炎症基因表达的影响，包括 NF-κB 的激活。辐射增强了 NF-κB 的激活，氧化应激导致氧化还原平衡的剂量依赖性破坏。本研究的意义在于通过 MAPK 信号通路，通过 NF-κB 激活促炎基因，获得了关于γ射线照射效应的新分子信息。考虑到 NF-κB 和其他促炎介质对氧化还原状态的高度敏感性，我们得出结论，辐射引起的炎症过程的激活可能是由氧化应激增加引起的。
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