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目的以小鼠肺组织中TGFβ1含量变化为指标,观测高低氧(HO+LO)照射对肺晚期损伤的生物学效应。方法雄性C57BL小鼠,13Gy全肺一次照射,照射同时分别吸入空气、高氧(95%O2+5%CO2)或高低氧(10%O2+5%CO2+85%N2),照射后不同时间取肺组织HE染色、Mason染色、V.G.染色观察肺纤维化形成。RTPCR方法测定肺组织内TGFβ1的表达。结果照射后8个月肺组织局部灶性纤维化形成。高氧组肺纤维化面积大于空气组及HO+LO组,两者相比,差异具有显著性;HO+LO组纤维化面积虽略高于空气组,但差异无显著性。照射后36小时,TGFβ1表达下降,照射后2个月,TGFβ1表达升高,至照射后8个月,略呈下降趋势,但仍高于正常对照。结论低氧的加入降低单纯高氧导致的正常组织损伤,HO+LO照射不增加肺的晚期损伤,TGFβ1的表达在肺纤维化形成过程中起重要作用
Objective To investigate the biological effects of high hypoxia (HO + LO) irradiation on the late lung injury in mouse lung tissue. Methods Male C57BL mice, 13 Gy whole lung single irradiation, irradiated simultaneously the intake air, high oxygen (95% O2 + 5% CO2) or high hypoxia (10% O2 + 5% CO2 + 85% N2), after irradiation at different time lung tissue HE Staining, Mason staining, V. G. Staining observed pulmonary fibrosis. RT PCR method for determination of TGF β1 expression in lung tissue. Results Pulmonary tissue focal fibrosis was formed 8 months after irradiation. The area of pulmonary fibrosis in hyperoxia group was larger than that in air group and HO + LO group, the difference was significant. The area of fibrosis in HO + LO group was slightly higher than that in air group, but the difference was not significant. 36 hours after irradiation, TGF β1 expression decreased 2 months after irradiation, TGF β1 expression increased to 8 months after irradiation, a slight downward trend, but still higher than the normal control. Conclusion The addition of hypoxia caused by high oxygen reduction simply damage to normal tissue, HO + LO advanced without increasing the irradiation damage to the lungs, during play an important role in the expression of pulmonary fibrosis formed TGFβ1