Role of p38 mitogen-activated protein kinase signal transduction pathway in the acute lung injury of severely burned rats.
- Author:
Xu-lin CHEN
1
;
Zhao-fan XIA
;
Duo WEI
;
Dao-feng BEN
;
Guang-qing WANG
;
Sheng HAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blotting, Western; Burns; enzymology; physiopathology; Enzyme Activation; drug effects; Enzyme Inhibitors; pharmacology; Imidazoles; pharmacology; Lung; pathology; physiopathology; Male; Mitogen-Activated Protein Kinases; antagonists & inhibitors; metabolism; physiology; Pyridines; pharmacology; Random Allocation; Rats; Rats, Sprague-Dawley; Respiratory Distress Syndrome, Adult; enzymology; physiopathology; Signal Transduction; drug effects; physiology; p38 Mitogen-Activated Protein Kinases
- From: Chinese Journal of Surgery 2004;42(7):388-390
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in the acute lung injury of severely burned rats.
METHODSForty-eight adult healthy rats were randomly divided into three groups: sham group, burn control group, and burn + SB203580 group. A third-degree burns over 30% total body surface area rat model was used and pulmonary capillary permeability, lung water content, pulmonary histology and p38 MAPK activity were measured at 24 hours postburn.
RESULTSBurn trauma resulted in increased pulmonary capillary leakage permeability (42.5 +/- 4.7 vs. 12.1 +/- 1.4, P < 0.01), elevated lung water content (P < 0.05), and worsen histologic condition. There was a significant activation of p38 MAPK at 24 hours postburn compared with control. SB203580 inhibited the activation of p38 MAPK, reduced the pulmonary capillary leakage permeability (24.7 +/- 2.9 vs. 42.5 +/- 4.7, P < 0.01), decreased lung water content, and prevented burn-mediated lung injury.
CONCLUSIONThe activation of p38 MAPK is one important aspect of the signaling event that contributes to burn-induced lung injury.
