Effect Of Hyperoxia On The Expression Of Cytochrome Oxidase In Premature Newborn Rat Lung

Objective Up to now, the pathogenesis of hyperoxia-induced lung injury has not been elucidated completely. Oxidative stress reaction is believed to play critical roles in the development of lung injury. This topic intends to observe the expression of mitochondrial encoding cytochrome oxidase genes in lungs of premature newborn rats exposed to 85﹪hyperoxia and explore the role of COX in hyperoxia-induced lung injury.Methods The one-day-old premature SD rats were randomly divided into air group and hyperoxia group. Hyperoxia group were continuously exposed to 85﹪oxygen and air group in room air. After 1,4,7,10,14 days of exposure, eight rats of each group were killed and total lung RNA were extracted. Expression of COXⅠ, COXⅡand COXⅢmRNA were detected by reverse transcription polymerase chain reaction (RT-PCR). Immunohistochemistry and Western-blot were used to detect COXⅠprotein.Results (1) expression of mRNA: COXⅠmRNA expression of the hyperoxia group was increased significantly at day 1 and day 4 compared with that of air-breathing control rats (P﹤0.05 and P﹤0.01). Since then it began to descend and there was no significant difference of COXⅠmRNA expression between the two groups at day 7(P﹥0.05). COXⅠmRNA expression of hyperoxia exposure decreased significantly at day 10 (P﹤0.01),but it was increased again at day 14 (P﹤0.01). The expression of COXⅡand COXⅢ mRNA between two groups has no significant difference. (2) COXⅠprotein expression of hyperoxia was increased significantly compared with age-matched room air control rats at day 1 and day 4 (P﹤0.01 and P﹤0.05). The differences of COXⅠexpression between the two groups were not significant at day 7 (P﹥0.05). Since then it began to descend, COXⅠe xpression of hyperoxia exposure was decreased significantly compared with air-breathing control rats at day 10 and day 14 (P﹤0.01 and P﹤0.05).Conclusion Exposure of 85﹪hyperoxia has significant impact on the expression of COXⅠin premature newborn rats, which is likely to contribute to the pathogenesis of hyperoxia-induced lung injury.