Changes of pulmonary surfactant protein A in young rats with acute lung injury induced by lipopolysaccharide.
- Author:
Lin-Hua SHU
1
;
Ke-Lun WEI
;
Chun-Feng LIU
;
Xiao-Hua HAN
;
Yun-Xiao SHANG
;
Xu-Xu CAI
;
Jiu-Jun LI
;
Li-Jie WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Female; Lipopolysaccharides; toxicity; Lung; chemistry; Male; Pulmonary Surfactant-Associated Protein A; analysis; Rats; Rats, Sprague-Dawley; Respiratory Distress Syndrome, Adult; metabolism
- From: Chinese Journal of Contemporary Pediatrics 2008;10(2):203-206
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEPulmonary surfactant protein A (SP-A) plays an important role in the maintenance of pulmonary surfactant function and innative immune defence. This study aimed to explore the changes of SP-A concentration in the lungs of young rats with acute lung injury.
METHODSSprague-Dawley rats were randomly assigned to control and lung injury groups. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the lung injury group. The same amount of normal saline was given for the control group. The two groups were subdivided into 6 groups sacrificed at 6, 12, 24, 36, 48 and 72 hrs of injection (n=8 each). Western blot was employed to detect SP-A concentration in the lung tissues.
RESULTSSP-A concentration in the lung injury group was not different from the the control group within 12 hrs after LPS injection. SP-A concentration in the lung injury group was elevated significantly during 24-48 hrs after LPS injection, peaking at 36 hrs (6.94+/-0.80 vs 5.01+/-0.36; P< 0.01), compared with the controls. However, SP-A concentration in the lung injury group was significantly reduced 72 hrs after LPS injection compared with the controls (P< 0.01).
CONCLUSIONSThe changes of lung SP-A concentration in rats following acute lung injury were time-dependent. The transient elevation of SP-A concentration in the lungs indicated a strong compensation ability of SP-A in the host defence against acute lung injury.