Expression of ERK1/2 protein in lung tissues of newborn rats with hyperoxia-induced chronic lung disease.
- Author:
Yu HU
1
;
Xue-Yan LIU
;
Jian-Hua FU
;
Xin-Dong XUE
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Chronic Disease; Female; Hyperoxia; complications; Lung; enzymology; pathology; Lung Diseases; etiology; metabolism; pathology; Male; Mitogen-Activated Protein Kinase 1; analysis; Mitogen-Activated Protein Kinase 3; analysis; Phosphorylation; Pulmonary Fibrosis; etiology; Rats; Rats, Wistar
- From: Chinese Journal of Contemporary Pediatrics 2011;13(7):581-585
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the expression of extracellular signal regulated protein kinase (ERK) 1/2 in lung tissues of newborn rats with chronic lung disease (CLD) caused by hyperoxia.
METHODSForty-eight full-term newborn rats were randomly divided into two groups: hyperoxia and control. The two groups were exposed to a hyperoxic gas mixture (0.90 O(2)) for an induction of CLD and room air within 12 hrs after birth, respectively. The levels of ERK1/2 protein and mRNA in lung tissues were measured using immunohistochemistry, Western blot and real-time PCR methods on postnatal days 3, 7 and 14. The severity of pulmonary fibrosis was evaluated.
RESULTSThe expression of p-ERK protein in lung tissues in the hyperoxia group was significantly higher than that in the control group on postnatal days 7 and 14 (P<0.01). There were no significant differences in the levels of total ERK1/2 protein and ERK1/2 mRNA.
CONCLUSIONSThe activation of phosphorated ERK1/2 may lead to lung fibrosis caused by hyperoxia in newborn rats.
