Abstract | PURPOSE: MATERIALS AND METHODS:
Hyperoxia-induced BPD in neonatal rats and hyperoxia-induced A549 cells were constructed. The mRNA expression of CDC2 was detected by qRT-PCR. The fibrosis score of lung tissues was evaluated by hematoxylin- eosin staining. The viability and apoptosis of A549 cells were detected by cell counting kit-8 assay and flow cytometry. The protein expressions of bcl-2, bax, and caspase-3 were measured by western blot. The levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β in A549 cells were detected by enzyme-linked immunosorbent assay. The pcDNA3.1-CDC2 was injected into rats to determine the role of CDC2 in hyperoxia-induced BPD in vivo. RESULTS: The expression of CDC2 was decreased in lung tissues of neonatal rats with hyperoxia-induced BPD and hyperoxia-induced A549 cells. The fibrosis score was increased in the lung tissues of neonatal rats with hyperoxia-induced BPD. Overexpression of CDC2 increased the viability and protein expression of bcl-2; and inhibited the apoptosis, inflammation, and protein expression of bax and caspase-3 in hyperoxia-induced A549 cells. Up-regulation of CDC2 alleviated the histopathologic changes in lung tissues of neonatal rats with hyperoxia-induced BPD. CONCLUSION: Overexpression of CDC2 promoted the viability and inhibited the apoptosis and inflammation of hyperoxia-induced cells, and alleviated the histopathologic changes of lung tissues in neonatal rats with hyperoxia-induced BPD.
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Authors | Zhongying Li, Yanhong Chen, Wenrong Li, Fan Yan |
Journal | Yonsei medical journal
(Yonsei Med J)
Vol. 61
Issue 8
Pg. 679-688
(Aug 2020)
ISSN: 1976-2437 [Electronic] Korea (South) |
PMID | 32734731
(Publication Type: Journal Article)
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Copyright | © Copyright: Yonsei University College of Medicine 2020. |
Chemical References |
- Cytokines
- Inflammation Mediators
- CDC2 Protein Kinase
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Topics |
- A549 Cells
- Animals
- Animals, Newborn
- Apoptosis
- Bronchopulmonary Dysplasia
(etiology, prevention & control)
- CDC2 Protein Kinase
(metabolism)
- Cell Cycle
- Cell Survival
- Cytokines
(metabolism)
- Disease Models, Animal
- Humans
- Hyperoxia
(complications, pathology)
- Inflammation Mediators
(metabolism)
- Lung
(pathology)
- Rats, Wistar
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