高体积分数氧致慢性肺疾病新生鼠信号转导转录活化因子3表达及其对表面活性蛋白-B的影响  

Expression of Signal Transducer and Activator of Transduction 3 and Their Contribution to Expression of Surfactant Proteins in Lung Tissue in Hyperoxia Induced Chronic Lung Disease in Newborn Rats

作　　者：岳冬梅[1] 佟雅洁[1] 薛辛东[1] 

机构地区：[1]中国医科大学附属盛京医院儿科,沈阳110004

出　　处：《实用儿科临床杂志》2011年第8期583-585,共3页Journal of Applied Clinical Pediatrics

基　　金：国家自然科学基金(30672253)

摘　　要：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 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（Pa0.05）.But no significant difference could be found in the experimental group 3 compared with that in the room-air control group（P0.05）.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（Pa0.05）.The expression of SP-B mRNA in the experimental group was positively related to the expression of STAT3 protein（r=0.892,P0.001）.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.

关 键 词：高体积分数氧 肺损伤 信号转导转录活化因子3 肺表面活性蛋白-B 

分 类 号：R563[医药卫生—呼吸系统]