Objective To investigate the expression of signal transducer and activator of transduction 3 ( STAT3 ) in the lung tissue under hyperoxia induced lung injury condition and their contribution to the expression of surfactant proteins( SP - B). Methods Newborn rats( 160 cases) were divided into 4 groups according to different oxygen concentrations( FiO2 ) :experimental group 1 (FiO2 =800 mL · L-1) ,experimental group 2( FiO2 =600 mL · L-1 ) ,experimental group 3( FiO2 =400 mL · L-1 ) and room -air control group ( FiO2 =210 mL · L-1 ).Rats were killed on the 1st ,3rd ,5th ,7th and 14th day after the onset of the experiment, and the expression of SP - B were examined by using reverse transcription polymerase chain reaction method. The expression of STAT3 in lung tissue were also determined by immunohistochemistry.Results High levels of oxygen exposure increased the SP - B mRNA expression and compared with the room - air control group significant diffe-rences could be found in the experimental group 1 on the 5th,7th and 14th day and in the experimental group 2 on the 5th day(Pa ＜0. 05). But no significant difference could be found in the experimental group 3 compared with that in the room - air control group ( P ＞0.05). From the 3rd day, the expression of STAT3 in the lung tissues in the experimental groups began to increase compared with that in room - air control group and the differences were much more remarkable on the 5th and 7th day ( pa ＜ 0. 05 ). The expression of SP - B mRNA in the experimental group was positively related to the expression of STAT3 protein ( r = 0. 892, P ＜ 0. 001 ). Conclusions At the early stage of hyperoxia induced lung injury, Janus kinase - STAT3 pathway can be activated to play a protective role and the stimulating signal for the synthesis and secretion of SP - B may be transmitted through STAT3 pathway.%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1 d、3 d、5 d、7 d、14 d,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1 d、3 d SP-B mRNA 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5 d、7 d、14 d 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5 d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,5 d、7 d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.
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