Expression Of STAT3 In The Lung Of Premature Neonatal Rats Exposed To Hyperoxia And Its Significance

OBJECTIVE:To master Signal transducer and activator of transcription 3(STAT3) expression in the lung of neonatal premature rats exposed to hyperoxia,and exploring the internal relationship with STAT3 of the chronic lung disease in preterm infants,and further elaborated the pathogenesy of the chronic lung disease in preterm infants.METHODS:102 neonatal Sprague-Dawley rats of 22-day gestational age were randomized into experimental group and control group,the neonatal rats in experimental group were fed in high concentration of oxygen(inhaled 95%oxygen) and the control groups were fed in the room air. According to the number random method eight neonatal SD rats were respectively extracted as corresponding subgroups at postnatal 3^th,7^th and 14^th day.After extraction,the neonatal rats were executed and got the lung tissues,observing the pathological diagnosis of lung tissues by HE stain. using Masson trichrome stain to assess the interstitial fibrosis severity of lung.The expression of STAT3 in lung tissues were analyzed by Immunohistochemical techniques.And also examined the expression of STAT3 messenger ribonucleic acid(mRNA) in rat lung by fluorescent real-time RT-PCR.RESULTS:1.Pathological change of lung tissues:We did not observe visible pathological change in air group at postnatal 3^th,7^th and 14^th day.A great deal of inflammatory cells effusion and thickened alveoli septum were observed in the lung tissues of 7^th hyperoxic group.Decreased Inflammatory cells's numbers and obvious destroyed alveolars,decreased number of alveoli,diverse alveolar size and marked thickened alveoli septum were observed in the hyperoxic group at postnatal 14^th day.2.The extent of lung fibrosis:Masson trichrome stain showed that collagen fibers did not increase in air group and increased markedly in hyperoxic group at postnatal 7^th day and aggravated until 14^th day.3.The expression of STAT3 protein and STAT3mRNA:The expression of STAT3 in alveolar and bronchi epithelial cells and vascular endothelial cells as well as inflammatory cells were stronger on the postnatal 3th,7^th and 14^th day in hyperoxic group,the difference was significant compared with air group,P＜0.05.The expression of STAT3mRNA in the lung of all groups were conformity,by fluorescent real-time RT-PCR technique(P＜0.05).CONCLUSIONS:Hyperoxic exposure can cause lung damage,inflammatory response is an early stage and the degree of fibrosis were increased gradually,furthermore along with the extension of oxygen uptake time that the pathological injuried were gradually increased.The lung tissue expression of STAT3 were increased with the extension of exposure time at early stage of hyperoxic group,it suggested that the STAT3 play a role in the early phase of acute inflammation and gradually reduced in the later fibrosis stage,it is not confirmed there was relationship with fibrosis at later stage of hyperoxia-induced lung injury.