ABSTRACT
OBJECTIVE: To establish dose-related lung inflammatory injury in rats model with intratracheal atomization of lipopo-lysaccharide (lipopolysaccharides, LPS). METHODS: Four groups of 4 rats were subjected to solvent or a single dose of LPS by in- tratracheal route using a IA-1B-2 inches-microsprayer. The male rats received 200 μL solvent (control), LPS solutions (15, 5, 0.5 mg·kg-1). All rats were sacrificed 24 h after dose administration, biochemical analysis and cell counts on bronchoalveolar lavage fluid (BALF) were performed on each rat. Lung, trachea and kidney were examined histologically. Serum chemistry profiles of creatinine, ALB, Na, K, Cl-were detected. RESULTS: Cell counts in BALF showed LPS groups had different degrees of inflammatory reaction. The alkaline phosphatase and total protein concentration were higher in LPS high dose group compared with other groups. In addition, the concentration of TNF-α increased consistently with LPS dose and has statistical significance compared with the control group. Histopathology findings demonstrated that LPS produced an accumulation of foamy macrophages in the lungs and high degree of inflammation. CONCLUSION: The results recommends intratracheally atomizing doses of LPS in rats model produced ranks of lung inflammatory injury.
ABSTRACT
Objective To investigate the expression of Na+/H + exchanger isoform-1 (NHE-1) during ischemia-reperfusion (IR)in rat lung tissue and determine whether cariporide preconditioning protects lung from inflammatory injury via inhibiting NHE-1 protein expression.Methods Twenty i-solated perfused lungs were randomly divided into 4 groups:the lungs in control group (group C) were continuously perfused for 120 min;the lungs in group IR were subjected to 30 min perfusion, followed by 60 min ischemia and 30 min reperfusion;in group LiCl preconditioning,the lungs were preconditioned with LiCl for 30 min,then continuously perfused for 90 min;in cariporide precondi-tioning+IR (CIR)group,the lungs were preconditioned with cariporide for 30 min,following 60 min ischemia and 30 min reperfusion.After reperfusion,the NHE-1 protein expression was determined by immunohistochemistry and the histopathologic change and pathology scores were ascertained from HE sections.Results The NHE-1 protein expression in lung tissue in groups IR and LiCl were signifi-cantly increased compared with groups C and CIR (P <0.05),and there was no difference between groups C and CIR.Histological examination revealed marked inflammatory changes in groups IR and LiCl,whereas no significant changes in lungs of groups C and CIR.The pathology score of lung in groups IR and LiCl were higher than that in groups C and CIR (P <0.05),and there was no differ-ence between the last two groups.Conclusion IR results in an increased NHE-1 protein expression in rat isolated perfused lung,and the selective NHE-1 inhibitor cariporide could repress the NHE-1 pro-tein expression,thereby decrease the lung inflammatory injury after IR.