摘要
目的研究氡吸入染毒小鼠肺及支气管组织中JNK／SAPK信号通路的表达变化。方法采用SR-NIM02型氡室对小鼠进行吸入染毒0．02、30和60工作水平月（WLM）），染毒结束后24h内处死；提取小鼠肺及支气管组织总RNA，利用Real—TimePCR定量分析JNKmRNA的表达水平；分别利用Westemblot和免疫组织化学技术检测肺及支气管组织中JNK蛋白表达及其磷酸化水平。结果Real—timePCR检测结果显示，染毒30与60WLM组的JNKmRNA水平分别是对照组的3．56倍和2．96倍（单因素方差分析，F=8．00，P〈0．05）；Westernblot结果显示，染毒30和60WLM组的JNK蛋白相对表达量分别为对照组的1．21和1．35倍（单因素方差分析，F=5．76，P〈0．05），JNK蛋白磷酸化水平分别为对照组的2．34和2．81倍（单因素方差分析，F=6．83，P〈0．05）；免疫组化结果显示，染毒后小鼠肺组织中JNK与胞核中磷酸化JNK蛋白表达增强。结论氡吸入染毒后可激活细胞内的JNK／SAPK信号通路，使其表达增强，并且磷酸化激活进入胞核，进而引起组织细胞的一系列反应。
Objective To study the expression of JNK/SAPK（ c-Jun NH2-terminal kinase/stress activated protein kinase） in lung and bronchus of radon-exposed mice. Methods Male BALB/c mice were exposed to radon and its progeny with the cumulative dose of 0.02, 30 or 60 working level month （WLM）, respectively. The expression levels of JNK/SAPK in lung and bronchus were determined with Real-Time PCR, Western blot and immunohistochemistry methods. Results The JNK mRNA levels in lung tissues of mice exposed to radon of 30 and 60 WLM were higher than those of the control by 3.56 and 2.96 times, respectively. The relative expression levels of JNK and phospho-JNK proteins were higher than those of the control by using Western blot and immunohistochemistry methods. Conclusions Expose to the radon and its progeny might activate the JNK/ SAPK intracellular signaling pathway.
出处
《中华放射医学与防护杂志》
CAS
CSCD
北大核心
2009年第2期192-195,共4页
Chinese Journal of Radiological Medicine and Protection
关键词
氡及其子体
小鼠
染毒
JNK/SAPK
Radon and its progeny
Mice
Exposure
JNK/SAPK （ c-Jun NH2-terminal kinase/ stress activated protein kinase）
