ABSTRACT
Objective To investigate the effect of sodium nitroprusside (SNP) , an exogenous NO donor, on expression of hemeoxygenase-1 (HO-1) and inducible NO synthase (iNOS) in the lung tissue in a rat model of lpopolysaccharide (LPS)-induced acute lung injury and the underlying mechanism.Methods Thirty-two Wistar rats of either sex weighing 190-210 g were randomly divided into 4 groups ( n = 8 each) : Ⅰ sham operation (S) ;Ⅱ LPS;Ⅲ hemin + LPS and Ⅳ SNP + LPS. The animals were anesthetized with intraperitoneal (IP) 7% chloralhydrate 5 ml?kg-1. LPS 750 ?g?kg-1 in 300 ?l was instilled into the lungs via trachea in group Ⅱ . In group Ⅲ hemin (a HO-1 inducer) 40 ?mol?kg-1 was injected IP 12 h before LPS. In group Ⅳ SNP 25 ?g?kg-1 + LPS 750 ?g?kg-1 in 300 ?l was instilled into the lungs via trachea. In group S normal saline 300 ?l was instilled via trachea instead of LPS. The animals were killed by (1) exsanguination from carotid artery 8h (2) after LPS instillation and lungs were removed for broncho-alveolar lavage (BAL) and detennination of protein concentration in BALF and the expression of HO-1 and iNOS protein in the lung tissue by immune-histochemical technique and HPIAS-2000 image analysis system and MDA content in lung tissue and (3) light microscopic examination (4) wet/ dry lung weight ratio.Results The 4 groups were comparable with respect to body weight and sex (M/F ratio) . The expression of iNOS and HO-1 in lung tissue was significantly higher in LPS group than in S group ( P
ABSTRACT
Objective:To study the effect of growth hormone(GH) on acute lung injury induced by endotoximia and its’ mechanism.Methods:After introduction of acute lung injury(ALI) by endotoximia,one hundred and tweleve male Sprague-Dawley rats were randomly divided into ALI group and GH group. Western blot,immunofluorescence staining and semi-quantitive reverse transcription polymerase chain reaction(RT-PCR) were used to determine the expression and activation of nuclear factor kappa B(NF-?B), the levels of CC16 protein and the expression levels of CC16 mRNA in ALI rats’ lung.Results:Both the expression levels of CC16 mRNA and the contents of CC16 protein in ALI rats’ lungs began to decrease significantly 0.5 h post-injury,reached nadir at 6 h post-injury,and then began to recover.Both the expression levels of CC16 mRNA and the contents of CC16 protein in GH group were significantly lower than those in ALI group at different time intervals post-injury.The dynamic changes of the expression and activation of NF-?B were contrast to those of CC16 protein levels.Correlation analysis indicated that CC16 correlates significantly with the extent of lung injury and the expression and activation of NF-?B.Conclusion:Down-regulation of CC16 expression plays a critical role in the pathogenesis of acute lung injury induced by endotoximia.The application of GH can deteriorate the lung injury induced by endotoximia through down-regulating the expression of CC16.