Animals ; Chronic Disease ; Disease Models, Animal ; Female ; Gene Expression Regulation, Developmental ; Hyperoxia ; Immunohistochemistry ; Lung ; growth & development ; metabolism ; Lung Diseases ; metabolism ; Oxygen ; Pregnancy ; RNA, Messenger ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Transforming Growth Factor beta1 ; genetics ; metabolism

Apoptosis ; physiology ; Bronchopulmonary Dysplasia ; physiopathology ; Chronic Disease ; Humans ; Infant, Newborn ; Infant, Premature ; Lung ; pathology ; physiopathology ; Receptors, Transforming Growth Factor beta ; physiology ; Transforming Growth Factor beta ; classification ; physiology

Objective To investigate the dynamic change of expression of cyclin dependent kinase-4(CDK4)and cyclin dependent kinase inhibitor(p21)in premature rats with hyperoxia-induced chronic lung disease(CLD)and its role.Methods Eighty premature rats were randomly and equally divided into model group(hyperoxia group)and control group(room air group).CLD was induced by hypemxia exposure.The expression of CDK4 and p21 were observed with immunohistochemical method,and the levels of type I collagen were detected by enzyme-linked immunosorbent assay on days 1,3,7,14 and 21.Results Compared with control group,in model group,the expression of CDK4 protein and level of type I collagen statistically increased,but expression of p21 protein decreased significantly on days 14 and 21.The expression of CDK4 was positive correlated with the degree of fibrosis,and expression of p21 was negative correlated with the degree of fibrosis in model group.Conclusion The expression of CDK4 increases and expression of p21 decreases in premature rats exposed to hyperoxia,which may play an important role in the lung fibrosis.

Adult ; Coronary Artery Disease ; complications ; etiology ; Female ; Heart Valve Prosthesis ; adverse effects ; Humans ; Mitral Valve ; surgery ; Myocardial Infarction ; etiology ; Postoperative Complications ; Thromboembolism ; complications ; etiology

Humans ; Hypoxia-Ischemia, Brain ; pathology ; Infant, Newborn ; Magnetic Resonance Imaging

Objective To explore the apoptosis of alveolar epithelial cell(AEC)and the dynamic changes of Caspase-3 mRNA and Bax and Bcl-2 expression in premature rat with hyperoxia-induced chronic lung disease(CLD).Methods Sixty premature rats within 1 day after birth were randomly divided into 2 groups:hyperoxia group(n=30)and control group(n=30).Hyperoxia-induced premature rat CLD models were prepared,and situ nick end-labeling(TUNEL),reverse transcription polymerasechain reaction(RT-PCR)and immunohistochemical technique were used to determine apoptosis index(AI)of AEC and the expressions of Caspase-3 mRNA and Bax and Bcl-2 proteins in lung tissues at 1,3,7,14 and 21 d after birth.Results Compared with control group,in the hyperoxia group,on the third day after exposured to hyperoxia,the AI of AEC and the expressions of Caspase-3 mRNA and Bax began to increase,and the expression of Caspase-3 mRNA was kept at high level on 7-21 d.The expression of Bcl-2 began to decrease on 7 d,and significantly decreased on 7-21 d.AI of AEC was positively correlated with the expression of Caspase-3 mRNA and Bax,and negatively with the expression of Bcl-2.Conclusions Hyperoxia may induce the increased expression of Caspase-3 mRNA,which might result in the abnormal expression of Bax and Bcl-2 in lung tissues and their imbalance,which might be one of the underlying mechanisms of apoptosis of AEC in premature rats with CLD.

0.05),and the expression of HoxB5 in the model group tapered after the 7th day,but the expression of HoxB5 increased and reached the peak on the 7th day and expressed in a stable level in the control group and were significantly higher than those of model group(Pa

Brain Injuries ; etiology ; Humans ; Hypoglycemia ; complications ; Infant, Newborn

Brain ; pathology ; Humans ; Infant, Newborn ; Lung ; pathology ; Male ; Seizures ; etiology ; pathology ; Tomography, X-Ray Computed ; Tuberous Sclerosis ; complications ; pathology