Effect of amygdalin on the proliferation of hyperoxia-exposed type II alveolar epithelial cells isolated from premature rat.
- Author:
Huaping ZHU
1
;
Liwen CHANG
;
Wenbin LI
;
Hanchu LIU
Author Information
1. Department of pediatric, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
- Publication Type:Journal Article
- MeSH:
Amygdalin;
isolation & purification;
pharmacology;
Animals;
Animals, Newborn;
Cell Hypoxia;
Cell Proliferation;
drug effects;
Cells, Cultured;
Dose-Response Relationship, Drug;
Epithelial Cells;
cytology;
drug effects;
Lung;
cytology;
metabolism;
Proliferating Cell Nuclear Antigen;
biosynthesis;
genetics;
Pulmonary Alveoli;
cytology;
drug effects;
Rats;
Rats, Sprague-Dawley
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2004;24(3):223-225
- CountryChina
- Language:English
-
Abstract:
The pathogenesis of hyperoxia lung injury and the mechanism of amygdalin on type 2 alveolar epithelial cells (AEC2) isolated from premature rat lungs in vitro were investigated. AEC2 were obtained by primary culture from 20-days fetal rat lung and hyperoxia-exposed cell model was established. Cell proliferating viability was examined by MTT assay after treatment of amygdalin at various concentrations. DNA content and the proliferating cell nuclear antigen (PCNA) protein expression of AEC2 were measured by using flow cytometry and immunocytochemistry respectively after 24 h of hyperoxia exposure or amygdalin treatment. The results showed that hyperoxia inhibited the proliferation and decreased PCNA protein expression in A-EC2 of premature rat in vitro. Amygdalin at the concentration range of 50-200 micromol/L stimulated the proliferation of AEC2 in a dose-dependent manner, however, 400 micromol/L amygdalin inhibited the proliferation of AEC2. Amygdalin at the concentration of 200 micromol/L played its best role in facilitating proliferation of AEC2s in vitro and could partially ameliorated the changes of proliferation in hyperoxia exposed AEC2 of premature rat. It has been suggested that hyperoxia inhibited the proliferation of AEC2s of premature rat, which may contribute to hyperoxia lung injury. Amygdalin may play partial protective role in hyperoxia-induced lung injury.
