The Expression And Effect Of CDK4,P21 In Lung Tissue In Premature Rats With Hyperoxia-induced CLD

IntroductionWith the development of neonatal intensive care technical and treatment, the premature infant survival rates have been visiblely improved, but chronic lung disease ( CLD ) in premature infant has a rising tendency in our country year by year. Its pathogenic mechanisms are not fully understood, at present there are not effective control methods or preventive measures which has influenced severly the quality of long - term living in premature infant .Although the pathogenic mechanism of CLD are not fully understood, the majority of research work in early days about CLD have already confirmed : the final pathological change are developmental disorder of alveoli of lung and lung fibrosis. Its pathoprocess is that various kinds etiological factor of CLD( such as higher level of supplemental oxygen , mechanical ventilation of high PIP and infection and so on ) can lead to pulmonary epithelial cells damage , remodeling and lung interstitial cell proliferation. Cell proliferation is regulated by cell cycle ,that can accommodate cell to run are cyclin dependent kinase(CDK) ,cyclin dependent kinase inhibitor (CDKI). At higher levels of supplemental oxygen whether cell cycle participle in lung cell proliferation is not clear, the relative researchs are less.The aim of the study were at investigating dynamic pulmonary morphology change and estimating lung fibrosis score and investigating dynamic proliferating cell nuclear antigen, cyclin dependent kinase and cyclin dependent kinase inhibitor in hyperoxia - inducedCLD in premature rats, to approach the relationship of the expression of CDK4 ,P21 and lung cell proliferation,we try to illuminate: the abnormal expression of CDK4 ,P21 are one of pathogenic mechanisms of lung...