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Objective@#To observe the expression of microRNA-125b (miR-125), tumor necrosis factor alpha (TNF-α) and interleukin-6(IL-6) in premature rats exposed to hyperoxia.@*Methods@#Eighty 1-day old Sprague Dawley (SD) rats were randomly divided into an air group and a hyperoxia group.The rats in the hyperoxia group were continuously exposed to oxygen chamber for 1-3 L/min, oxygen volume fraction was maintained at (800±50) mL/L, and the rats in air group were placed in the same room with the oxygen volume fraction at 210 mL/L.The feeding conditions were same in 2 groups.Lung tissues of premature rats were extracted at different time (1, 4, 7, 10, 14 days). The pathologic changes in the lung tissues were observed by hematoxylin-eosin (HE) staining.The levels of miR-125b and TNF-α, IL-6 in lung tissues were detected by reverse transcription polymerase chain reaction (qRT-PCT) and enzyme-linked immunosorbent assay (ELISA).@*Results@#Compared with the air group, miR-125b in the hyperoxia group increased slowly after day 1, reached the highest in day 10 (2.554±0.323), and the relative expression in day 14 decreased slightly(2.329±0.263), and there were significant differences between 2 groups at di-fferent time (all P<0.05); in particular TNF-α level increased in day 7 [(78.55±39.53) ng/L], and reached the peak at day 10 [(80.16±11.24) ng/L], and there was a significant difference(P<0.05); IL-6 levels increased at day 7 [(45.44±31.94) ng/L], and reached the peak at day 10 [(90.38±8.24) ng/L], and there was a significant difference(P<0.05). There was a no significant correlation between miR-125b and TNF-α in the hyperoxia groups (r=0.132, P>0.05), but there was significant correlation between miR-125b and IL-6 in hyperoxia groups(r=0.439, P<0.05).@*Conclusions@#The levels of miR-125b, TNF-α and IL-6 are involved in the pathological process of bronchopulmonary dysplasia induced by hyperoxia, and IL-6 may be the key factor for miR-125b.
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Objective To investigate the role of DRP1 and OPA1 in the process of apoptotic in hyperoxia induced lung injury of premature rats .Methods 48 premature Wistar rats were divided into control group in which rats were exposed tO 210 ml .L 1 oxy-en ,and hyperoxia group in which Rats were exposed to 950 mL .L 1 oxyen .The lung tissues of 2 groups were gained on the first day ,the second day and the seventh day with which that all mice were killed by cutting neck .Section of lungs were stained with hea-toxylin eosin to observe the pathological changes ,the protein expression in the lung cells which were linked with the change of plas-tosome ,then the premature rat lung tissue apoptosis in each group were evaluated .Results Compored with the contnx group ,the expression level of OPA1 in the hyperoxia group began to decrease on the first day and apparently decreased to the buttom line on the seventh day .On the other hand ,DRP1 in hyperoxia group began to increase on the first day ,while reached the summit on the seventh day .A few of TUNEL positive cells began to increase with time dependence .A lot of TUNEL positive cells could be found in hyperoxia group ,and the apoptotic index reached the peak on the 7 d .There is a significantly positive correlation between the cell apoptosis and the ratio change of DRP1 and OPA1 in high oxygen group(r=0 .725 ,P<0 .01) .Conclusion The classical pathologic characters of lung injury were found out in hyperoxia group ,and it changed obviously with time .
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Objective To explore the roles of Notch2,Notch4 in hyperoxia induced lung injury in premature rats.Methods At the postnatal 1 day Sprague-Dawley premature rats were randomly assigned to about 85% hyperoxia group and air group.At the 1,7,14,21 days after exposed,8 rats of each group were used to evaluate expressions of Notch2,Notch4 in lungs by immunohistochemistry and the level of Nothch2,Notch4 mRNA by reverse transcription polymerase chain reaction(RT-PCR).Results Expressions of Notch2,Notch4 had their rules in rats′ different stages of development;85% oxygen exposed would change their tracks.Conclusion Prolonged 85% oxygen exposure result in abnormal expressions of Notch2 and Notch4 ,which is likely to lead to the pathogenesis of hyperoxic lung injure in premature rats.