The Interventional Effect Of PGE1 On ERS Pathway With Hyperoxic Lung Injury In Neonatal Rats

Objective:To investigate the interventional effect of prostaglandin E1(PGE1)on endoplasmic reticulum stress(ERS)pathway with hyperoxia lung injury in neonatal rats.Methods:A total of 120 Wistar neonatal rats were randomly divided into three groups:the control group(n=40,Fi02=21%),the model group(n=40,Fi02>85%)and the treatment group(n=40,Fi02>85%).In the treatment group,PGE-1 2ug/(kg.d)was injected intraperitoneally from first days,and the other two groups were intraperitoneally injected with the same dose of saline.The 1d,3d,7d and 14d by weight of newborn rats;detection of lung tissue wet/dry ratio(W/D);pathological changes of lung tissue were observed by HE staining and TUNEL staining to observe cell apoptosis;lung;observation of inflammatory cells in bronchoalveolar lavage fluid were detected by Diff-quike staining;the content of ELISA in lung tissue of IL-1 beta TNF-,IL-6 and alpha;the expression of Caspase-12,GADD153,GRP78,JNK,pJNK and Bcl-2/Bax protein in lung tissue were measured by Westernblot methodResults:1.Compared with the control group,the weight of 1d,3d,7d and 14d in the model group decreased significantly(P<0.05),and the weight of the neonatal rats in the treatment group was significantly higher than that in the model group(P<0.05).2.The W/D values of Id,3d,7d and 14d in the neonatal rats in the model group,were higher than those in the control group(P<0.05).The values of lung W/D in the neonatal rats were significantly lower than those in the model group(P<0.05).3.Compared with the control group,the pathological changes of lung tissue in the model group were more obvious with the prolongation of hyperoxia exposure,and the pathological changes in the treatment group were less than that in the model group.4.With the prolongation of hyperoxia time,the apoptosis and inflammatory cells were more severe in the model group than in the control group(P<0.05).The apoptosis and inflammatory cells in the treatment group were significantly lower than those in the model group(P<0.05).5.Compared with the control group,the content of IL-1 beta,IL-6 and TNF-alpha in the lung homogenate of the model group was significantly increased(P<0.05).Compared with the model group,the content of IL-1 beta,IL-6 and TNF-alpha in the treatment group was significantly decreased(P<0.05).6.The expression of Caspase-12,GADD153,GRP78,JNK,pJNK protein in model group was significantly higher than that of control group(P<0.05),the expression of Bcl-2 was significantly lower(P<0.05),while the expression of Bax increased slightly,but there was significant difference(P<0.05);the expression of Caspase-12 of the treatment group,GADD153,GRP78 pJNK,JNK,and Bax protein significantly decreased as compared with model group(P<0.05),and Bcl-2 protein content increased significantly(P<0.05).Conclusions:1.PGE-1 can reduce the edema and inflammatory response in the lung tissue of neonatal rats induced by hyperoxia,and relieve the apoptosis of lung injury in neonatal rats induced by hyperoxia.2.The protective effect of PGE1 on hyperoxic lung injury may be related to the expression of Caspase-12,GADD153,GRP78,JNK,pJNK,Bax and Bcl-2 through the ERS pathway.