摘要
目的研究组蛋白H2AX在高氧致肺损伤新生大鼠肺组织中的表达,并探讨其在高氧肺损伤中的作用。方法将80例新生大鼠随机分为实验组(高氧组)和对照组(空气组),建立高氧致新生大鼠肺损伤的模型,在实验开始后1、2、3、5、7天取肺组织标本,运用免疫荧光技术和Western-blot方法检测高氧肺损伤过程中H2AX的表达规律。结果实验组大鼠肺组织H2AX蛋白平均荧光强度在实验开始后第1、2、3天(P<0.01)和第5天(P<0.05)明显高于对照组,第7天与对照组无明显差异(P>0.05);实验组H2AX蛋白平均荧光强度呈逐渐下降趋势(F=45.02,P<0.01),在第7天时接近对照组水平。H2AX蛋白相对表达量变化趋势与免疫荧光法结果相同,实验开始后第1天明显升高,并随着暴露高氧时间的延长逐渐降低。结论 H2AX可能与高氧致急性肺损伤密切相关。
Objective To explore the expression of I-I2AX in new born rats lung with hyperoxia-induced lung injury. Methods Eighty new born rats were randomly exposed to hyperoxia （model group ） and to room air（control group, n = 40 each ）. Lung injury was induced by hyperoxia exposure, the expression of H2AX was detected by immunofluorescence technique and Western-blot at 1, 2, 3 , 5 and 7 days after exposure. Results Average intensity of H2AX protein in new born rats of model group was increased significantly compared with the control group at the days 1,2,3 （P 〈0.01 ） and 5 （P〈 0.05 ） after hyperoxia exposure, but not for the 7th day （ P〉 0.05）, H2AX average intensity decreased with the time of hyperoxia exposure going on （F=45.02, P〈O.01） in the model group. H2AX relative expression was consistant with the result of average intensity, increased quickly in model group and decreased graduly with the length of time exposure to hyperoia compared with the control group. Conclusions H2AX is closely related to the development of hyperoxia induced lung injury probably.
出处
《解剖科学进展》
CAS
2011年第3期211-214,218,共5页
Progress of Anatomical Sciences
基金
国家自然科学基金资助项目(No.30872781)
