Relationship between expression of aquaporin-1, -5 and pulmonary edema in hyperoxia-induced lung injury in newborn rats.
- Author:
Dong-Mei YUE
1
;
Xin-Dong XUE
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Aquaporin 1; analysis; Aquaporin 5; analysis; Bronchoalveolar Lavage Fluid; chemistry; Female; Hyperoxia; metabolism; Lung; chemistry; Male; Pulmonary Edema; etiology; Rats; Rats, Wistar
- From: Chinese Journal of Contemporary Pediatrics 2006;8(2):147-150
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEAquaporin (AQP) is a group of cell membrane transporting proteins. The study was designed to investigate the changes of AQP1 and AQP5 in the lung tissue under hyperoxia and their roles in pulmonary edema.
METHODSTwo hundred newborn rats were randomized into different oxygen concentrations exposure: FiO2=0.80 (Experimental group 1), FiO2=0.60 (Experimental group 2), FiO2=0.40 (Experimental group 3) and FiO2=0.21 (Air control group). Rats were sacrificed at 1, 3, 5, 7 and 14 days after the beginning of experiment (10 rats each time point). The expressions of AQP1 and AQP5 were examined by Western Blot. The ratio of lung wet weight to lung dry weight (wet-to-dry weight ratio, W/D), and the protein content in bronchoalveolar lavage fluid (BALF) were measured.
RESULTSCompared with the Air control group, the W/D ratio and the protein content in BALF in the three experiment groups increased significantly and the increased extent was positively related to the duration and the oxygen concentration of hyperoxia-exposure. The expression of AQP1 in the experimental groups began to decrease at the 3rd day and significant differences were found at the 5th and the 7th days after hyperoxia-exposure compared with that in the Air control group (P < 0.05). The AQP1 expression was restored somewhat at the 14th day after hyperoxia-exposure, but it was still lower in the Experimental groups 1 and 2 than that in the Air control group (P < 0.05). The expression of AQP5 in the experimental groups were reduced compared with that in the Air control group 3 days after hyperoxia-exposure and the decrease of AQP5 expression was associated with duration of hyperoxia-exposure. The comparison among three experimental groups showed that the decrease of AQP1 and AQP5 expressions was associated with the concentration of hyperoxia-exposure.
CONCLUSIONSThe expressions of AQP1 and AQP5 decreased in hyperoxia-induced lung injury and correlated with the severity of pulmonary edema.