The Role Of Omi/Htra2in Lung Injury Of Premature Rats Exposed To Hyperoxia

Objective:The role of Omi/HtrA2in hyperoxia-induced lunginjury of premature rats were investigated.Methods:Prematre Wistar ratswere randomly divided into control group and hyperoxia group (24rats ineach group).The lung tissue in two group was obtained at1,3and7daysafter exposing room air and hyperoxia. Section of lungs was stainedwith HE to observe the histologic changes.Streptavidin-peroxidaseimmunohistochemistry was used to detect the expression ofOmi/HtrA,XIAP and caspase-9in the lung cell of each group.TUNELwas used to detect the apopotsis of lung cell.The translocation rate ofOmi/HtrA2were determined by indirect immunofluorescence andobserved under confocal microscopy. Results:Rats in hyperoxia groupshowed typical lung injury,which was characterized by alveolitis anddelayed of luny development. Omi/HtrA XIAP and caspase-9expressedgenerally in the cytoplasm of lung tissue.Compared with the controlgroup, the expression of Omi/HtrA and caspase-9began to increasefrom1day hyperoxia and was singnificantly increased in the3dayhyperoxia and peaked at7day hyperoxia（Omi/HtrA average optial： 1d5.19±0.39vs6.71±1.40、3d4.60±0.90vs9.69±0.96、7d5.38±0.46vs12.66±1.17）（1d、3d P<0.05、7d P<0.01）（,caspase-9averageoptial：1d3.58±1.39vs6.55±1.32、3d3.40±1.35vs11.29±2.48、7d3.76±1.71vs16.45±2.49）（1d、3d、7d P<0.01）. The expression of IAPbegan to decrease from1day hyperoxia and singnificantly decrease in the3and7day hyperoxia(Apoptotic index:1d14.61±2.00vs25.12±2.93、3d14.78±3.18vs44.09±3.26、7d14.63±2.25vs55.45±3.31).A few ofTUNEL-positive cells began to increase from1day hyperoxia and peakedat7day hyperoxia.Using Immunofluorescence,we confirmed thatOmi/HtrA could be significantly translocated to cytosol（translocationrate:1d6.35±0.64vs23.00±2.64、3d7.12±0.75vs38.77±2.42、7d7.67±0.96vs53.76±2.93).Conclusion:Omi/HtrA2could promotehyperxia-induced lung cell apoptosis in premature rats through inhibitingthe expression and activation of XIAP an activating ofcaspase-9,advavancing the injury of lung.