论文部分内容阅读
[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 the effect of radon on the expression of mitochondrial transcription factor A (TFAM) and nuclear factor (NF) -κB in lung tissues of mice and provide experimental evidence for exploring the mechanism of radon-induced lung injury. [Methods] Twenty healthy female BALB / c mice were randomly divided into control group and three groups with five radon groups. Radon exposures were 30,60 and 120 working months respectively. Mice were sacrificed within 1 h after the last exposure. HE staining and TFAM and NF-κB p65 immunohistochemical staining were performed on the lungs. Western blot was used to detect the protein expression of TFAM and NF-κB p65 in the lung tissue. [Results] The results of immunohistochemistry showed that the number of TFAM and NF-κB p65 positive cells increased significantly after radon exposure. The rates of TFAM and NF-κB p65 positive cells in month of 120 working level were (0.521 ± 0.081)% and (0.260 ± 0.068)%] higher than that in the control group [(0.093 ± 0.011)%, (0.069 ± 0.016)%, P <0.05]. Western blot also showed that the protein expression was also significantly increased. [Conclusion] The up-regulation of TFAM and NF-κB in lungs exposed to radon exposure suggests that NF-κB signaling pathway is activated.