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目的探讨高体积分数氧(高氧)损伤状态下,肺组织内信号转导转录活化因子3(STAT3)的动态变化规律,及其对表面活性蛋白-B(SP-B)的影响。方法新生鼠160只,依据吸氧体积分数(FiO2)分为4组:实验1组(FiO2=800 mL·L-1)、实验2组(FiO2=600 mL·L-1)、实验3组(FiO2=400 mL·L-1)、空气对照组(FiO2=210 mL.L-1)。每组分别于实验1d、3d、5d、7d、14d,免疫组织化学检测STAT3水平,反转录-PCR检测SP-B水平。结果高氧暴露使SP-B mRNA表达异常,实验1组1d、3d SP-BmRNA水平与空气对照组比较差异均无统计学意义(Pa>0.05),实验1组5d、7d、14d SP-B mRNA水平与空气对照组比较差异均有统计学意义(Pa<0.05),实验2组5d时SP-B mRNA水平与空气对照组比较差异有统计学意义(P<0.05),实验3组与空气对照组差异无统计学意义(P>0.05)。实验各组肺组织STAT3蛋白的表达高氧刺激3 d明显增加,5d、7d差异更为显著(Pa<0.05)。实验组SP-B mRNA表达与STAT3呈明显正相关(r=0.892,P<0.001)。结论高氧肺损伤的早期伴随有信号转导酪氨酸蛋白激酶STAT3通路的激活发挥其对肺组织的保护作用,SP-B合成、分泌信号可能是STAT3途径转导的。
Objective To investigate the dynamic changes of signal transducers and activators of transcription 3 (STAT3) and its effect on surfactant protein-B (SP-B) in lung tissues under high volume fraction of oxygen (hyperoxia) injury. Methods 160 neonatal rats were divided into 4 groups according to FiO2: FiO2 = 800 mL·L-1, FiO2 = 600 mL·L-1, (FiO2 = 400 mL · L-1), air control group (FiO2 = 210 mL.L-1). The levels of STAT3 in each group were detected by immunohistochemistry on day 1, day 3, day 5, day 7, day 14, and SP-B by reverse transcription-PCR. Results The expression of SP-B mRNA was abnormal in hyperoxia group. There was no significant difference in the level of SP-B mRNA on day 1 and day 3 between experimental group 1 and control group (P> 0.05) (P <0.05). The level of SP-B mRNA in experimental group 2 at 5 d was significantly lower than that in air control group (P <0.05), and that in experimental group 3 was significantly lower than that in air control group There was no significant difference in the control group (P> 0.05). The expression of STAT3 protein in lung tissue of experimental groups increased significantly after 3 days of hyperoxia stimulation, and the difference was more significant at 5 and 7 days (P <0.05). The expression of SP-B mRNA in experimental group was positively correlated with STAT3 (r = 0.892, P <0.001). Conclusion The activation of signal transduction tyrosine kinase kinase STAT3 pathway in early stage of hyperoxia-induced lung injury exerts its protective effect on lung tissue. The signal of SP-B synthesis and secretion may be transduced by STAT3 pathway.