氡诱发小鼠肺损伤与P53和Bcl-2、Bax蛋白表达的研究

目的 建立氡染毒小鼠肺损伤模型,观察不同剂量组小鼠肺组织损伤情况,分析氡对P53、Bcl-2、Bax在肺组织中表达的影响。方法 建立氡染毒小鼠模型,使染毒累积剂量分别达到30工作水平月(WLM)和60WLM;采用TUNEL法检测小鼠肺组织细胞凋亡程度;采用免疫组化SP法及Westernblot法,检测各组肺组织P53、Bcl-2、Bax蛋白表达情况。结果 与正常对照组相比,氡染毒30和60WLM小鼠肺细胞凋亡指数均明显增加(t=18.11、-10.30,P<0.05);氡染毒30WLM组P53蛋白明显增加(t=-11.08,P<0.05);60WLM组P53蛋白和Bax蛋白表达明显增加(t=-7.00、-2.52,P<0.05),Bcl-2蛋白表达明显下降(t=4.36,P<0.05);氡染毒30和60WLM与对照组相比,Bcl-2、Bax比值均明显下降(t=2.78、4.07,P<0.05)。结论 氡染毒可使小鼠肺损伤,出现肺细胞凋亡,P53、Bcl-2、Bax途径可能参与了肺细胞的凋亡调节。

Radon induced pulmonary lesion and expression of P53 and Bcl-2,Bax in mice

Objective To establish the mice model of lung injury induced by radon,and to observe the changes of pulmonary lesion at different doses and to analyze the influence of radon exposure on P53 and Bcl-2、Bax expression in lung tissue.Methods Mice were exposed to radon of 30 and 60 WLM,respectively.Apoptosis was detected by terrainal deoxynucleotidy transferse-mediated dUTP-biotin nick end labeling(TUNEL).The expressions of P53,Bcl-2 and Bax protein were observed by immunohistochemistry and Western blot.Results Compared with those in the control group,the apoptotic indexes increased significantly in the 30 and 60 WLM groups(t=18.11,-10.30,P＜0.05).The protein expression of P53 was significantly increased(t=-11.08,P＜0.05).The expression levels of P53 and Bax were remarkably inereased(t=-7.00,-2.52,P＜0.05),while the expression of Bcl-2 protein was significantly decreased in the 60 WLM group(t=4.36,P＜0.05).But Bcl-2,Bax expression was decreased in both 30 WLM and 60 WLM groups(t=2.78,4.07,P＜0.05).Conclusions Radon could induce pulmonary lesion of mice.It may be involved in the regulation of apoptosis of pulmonary lesion by the P53,Bcl-2、Bax pathway.