Apoptosis of Alveolar Epithelial Cell and Its Mechanism in Premature Rat with Hyperoxia-Induced Chronic Lung Disease
- VernacularTitle:高体积分数氧致慢性肺疾病早产鼠肺上皮细胞凋亡及其调控机制
- Author:
xiao-hong, YUE
;
jian-hua, FU
;
xin-dong, XUE
- Publication Type:Journal Article
- Keywords:
hyperoxia;
chronic lung disease;
cell apoptosis;
Caspase-3;
B cell lymphoma/leukemia-2 associated X protein;
B cell lyinphoma/leukemia-2
- From:Journal of Applied Clinical Pediatrics
1986;0(02):-
- CountryChina
- Language:Chinese
-
Abstract:
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.
