[Expression of ERK1/2 protein in lung tissues of newborn rats with hyperoxia-induced chronic lung disease].
Yu Hu, Xueyan Liu, Jianhua Fu, Xindong Xue
Abstract
Yu Hu, Xueyan Liu, Jianhua Fu, Xindong Xue
Abstract
OBJECTIVE: To 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. METHODS: Forty-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. RESULTS: The 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. CONCLUSIONS: The activation of phosphorated ERK1/2 may lead to lung fibrosis caused by hyperoxia in newborn rats.
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OBJECTIVE: To 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. METHODS: Forty-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. RESULTS: The 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. CONCLUSIONS: The activation of phosphorated ERK1/2 may lead to lung fibrosis caused by hyperoxia in newborn rats.
Key concepts: Hyperoxia, Lung, Western blot, Immunohistochemistry, Medicine, Messenger RNA, Bronchopulmonary dysplasia, Pulmonary fibrosis