中华放射医学与防护杂志
中華放射醫學與防護雜誌
중화방사의학여방호잡지
Chinese Journal of Radiological Medicine and Protection
2009年
2期
195-198
,共4页
朴春南%田梅%刘建香%阮健磊%郭志英%苏旭
樸春南%田梅%劉建香%阮健磊%郭誌英%囌旭
박춘남%전매%류건향%원건뢰%곽지영%소욱
氡%肺损伤%细胞凋亡%P53蛋白%Bcl-2蛋白%Bax蛋白
氡%肺損傷%細胞凋亡%P53蛋白%Bcl-2蛋白%Bax蛋白
동%폐손상%세포조망%P53단백%Bcl-2단백%Bax단백
Radon%Lung lesion%Apoptosis%P53 protein%Bcl-2 protein%Bax protein
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60 WLM;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60 WLM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30 WLM组P53蛋白明显增加(t=-11.08,P＜0.05);60 WLM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60 WLM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.
目的 建立氡染毒小鼠肺損傷模型,觀察不同劑量組小鼠肺組織損傷情況,分析氡對P53、Bcl-2、Bax在肺組織中錶達的影響.方法 建立氡染毒小鼠模型,使染毒纍積劑量分彆達到30工作水平月(WLM)和60 WLM;採用TUNEL法檢測小鼠肺組織細胞凋亡程度;採用免疫組化SP法及Westernblot法,檢測各組肺組織P53、Bcl-2、Bax蛋白錶達情況.結果 與正常對照組相比,氡染毒30和60 WLM小鼠肺細胞凋亡指數均明顯增加(t=18.11、-10.30,P＜0.05);氡染毒30 WLM組P53蛋白明顯增加(t=-11.08,P＜0.05);60 WLM組P53蛋白和Bax蛋白錶達明顯增加(t=-7.00、-2.52,P＜0.05),Bcl-2蛋白錶達明顯下降(t=4.36,P＜0.05);氡染毒30和60 WLM與對照組相比,Bcl-2、Bax比值均明顯下降(t=2.78、4.07,P＜0.05).結論 氡染毒可使小鼠肺損傷,齣現肺細胞凋亡,P53、Bcl-2、Bax途徑可能參與瞭肺細胞的凋亡調節.
목적 건립동염독소서폐손상모형,관찰불동제량조소서폐조직손상정황,분석동대P53、Bcl-2、Bax재폐조직중표체적영향.방법 건립동염독소서모형,사염독루적제량분별체도30공작수평월(WLM)화60 WLM;채용TUNEL법검측소서폐조직세포조망정도;채용면역조화SP법급Westernblot법,검측각조폐조직P53、Bcl-2、Bax단백표체정황.결과 여정상대조조상비,동염독30화60 WLM소서폐세포조망지수균명현증가(t=18.11、-10.30,P＜0.05);동염독30 WLM조P53단백명현증가(t=-11.08,P＜0.05);60 WLM조P53단백화Bax단백표체명현증가(t=-7.00、-2.52,P＜0.05),Bcl-2단백표체명현하강(t=4.36,P＜0.05);동염독30화60 WLM여대조조상비,Bcl-2、Bax비치균명현하강(t=2.78、4.07,P＜0.05).결론 동염독가사소서폐손상,출현폐세포조망,P53、Bcl-2、Bax도경가능삼여료폐세포적조망조절.
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.
