Expression of heme oxygenase-1 and inducible nitric oxide synthase in the lungs of hyperoxia-exposed preterm rats.
- Author:
Yu-Feng QUAN
1
;
Ming-Ci ZHENG
;
Hua ZHANG
;
Pei-Lin ZHANG
;
Hong ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Bronchoalveolar Lavage Fluid; chemistry; Female; Heme Oxygenase (Decyclizing); analysis; physiology; Hyperoxia; complications; enzymology; Lung; enzymology; Lung Injury; etiology; Male; Nitric Oxide Synthase Type II; analysis; physiology; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Contemporary Pediatrics 2011;13(7):577-580
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the expression and the role of heme oxygenase-1 (HO-1) and inducible nitric oxide synthase (iNOS) in preterm rats with hyperoxia-induced lung injuries.
METHODSSixty-four three-day-old preterm Sprague-Dawley rats were randomly assigned to a hyperoxia group (90% oxygen exposure) and a control group (room air exposure), with 32 rats in each group. After 3 days or 7 days of exposure, the lung activity of HO-1 and nitric oxide (NO) contents in bronchoalveolar lavage fluid (BALF), pulmonary histopathologic changes, and the cellular distribution and expression of HO-1 and iNOS in the lungs were measured.
RESULTSAfter 3 days and 7 days of exposure, the hyperoxia group showed acute lung injuries characterized by the presence of hyperaemia, red cell extravasation and inflammatory infiltration. The NO contents in BALF and the iNOS expression in the lungs increased significantly in the hyperoxia group compared with those in the control group 3 and 7 days after exposure. The expression of HO-1 in macrophages in the lungs increased significantly in the hyperoxia group compared with that in the control group 3 and 7 days after exposure. The NO contents in BALF and the iNOS and HO-1 expression in the lungs increased significantly 7 days after hyperoxia exposure compared with 3 days after hyperoxia exposure.
CONCLUSIONSiNOS and HO-1 levels in the lungs increase in preterm rats with hyperoxia-induced lung injuries, suggesting that iNOS and HO-1 may play roles in hyperoxia-induced pulmonary injuries.