Expression and role of p38 mitogen-activated protein kinase in hyperoxia-induced lung injury juvenile rat model.
- Author:
Jing LI
1
;
Feng XU
;
Lan HU
;
Li-Ping TAN
;
Yue-Qiang FU
;
Fang FANG
;
Feng-Wu KUANG
;
Zhong-Yi LU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Disease Models, Animal; Female; Hyperoxia; complications; Imidazoles; therapeutic use; Immunoblotting; Lung Injury; drug therapy; enzymology; etiology; MAP Kinase Signaling System; Male; Phosphorylation; Pyridines; therapeutic use; Rats; Rats, Wistar; p38 Mitogen-Activated Protein Kinases; analysis; physiology
- From: Chinese Journal of Contemporary Pediatrics 2009;11(5):389-392
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVESome research has shown that p38 mitogen-activated protein kinase (p38MAPK) plays important roles in lung injuries induced by various factors. Its expression and role in hyperoxia-induced lung injury remains unknown. This study investigated the expression and role of p38MAPK in hyperoxia-induced lung injury juvenile rat model.
METHODSHyperoxia-induced lung injury rat model was prepared by 90% O(2) exposure. The location and expression of p38MAPK in lung tissues were detected by immunohistochemistry and Western blot respectively. Apoptosis index of lung was evaluated by TUNEL technique. The effect of SB203580, a p38MAPK inhibitor, on the apoptosis index of lung was observed.
RESULTSThe expression of phosphor-p38MAPK increased obviously after hyperoxia. Positive phosphor-p38MAPK cells were mainly distributed in the alveolar, airway epithelial cells, pulmonary vascular endothelium cells and infiltrative inflammatory cells. The apoptosis index of lung also significantly elevated. SB203580 inhibited the activation of p38MAPK, and reduced the apoptosis index of lung.
CONCLUSIONSThe phosphor-p38MAPK increased and was expressed in many kinds of lung cells in lung injury rat model. It may play a role in the induction of apoptosis in hyperoxia-induced lung injury.
