[目的]观察氡对小鼠肺组织线粒体转录因子A(TFAM)及核因子(NF)-κB表达的影响,为探讨氡致肺损伤的机制提供实验依据。[方法]20只健康雌性BALB/c小鼠随机分为对照组及3个染氡组,每组5只,染氡组氡暴露剂量分别为30、60、120工作水平月。末次染毒后1 h内处死小鼠,取肺组织进行HE染色以及TFAM和NF-κB p65免疫组化染色,Western blot检测肺组织中TFAM和NF-κB p65的蛋白表达。[结果]免疫组化结果显示,染氡后TFAM、NF-κB p65阳性细胞数显著增加,其中120工作水平月组的TFAM和NF-κB p65阳性细胞率[(0.521±0.081)%、(0.260±0.068)%]高于对照组[(0.093±0.011)%、(0.069±0.016)%,P〈0.05],Western blot结果显示其蛋白表达也显著上升。[结论]氡暴露小鼠肺组织中TFAM和NF-κB的表达上调,提示NF-κB的信号通路被激活。
[Objective] To observe changes in expression of mitochondrial transcription factor A(TFAM) and nuclear factor kappa B(NF-κB) in mouse lung tissue induced by radon, so as to provide experimental evidence for understanding related mechanism. [Methods] Twenty healthy female BALB/c mice were randomly divided into one control group and three experimental groups with cumulative doses of radon at 30, 60, and 120 working level months(WLM). All mice were sacrificed 1 h after last treatment. The lung tissues were stained with HE, and the expressions of TFAM and NF-κB p65 were detected by immunohistochemistry and Western blot. [Results] The immunohistochemistry results showed that the positive cell rates of TFAM and NF-κB p65 significantly increased after radon exposure, and the 120 WLM group presented higher positive cell rates of TFAM and NF-κB p65 [(0.521±0.081)%,(0.260±0.068)%] than the control group [(0.093±0.011)%,(0.069±0.016)%, P 0.05]. So did the expression of protein according to Western blot. [Conclusion] The elevated expressions of TFAM and NF-κB induced by radon indicate an activation of NF-κB signaling pathway.