AIM: To establish the model of systemic inflammatory response syndrome (SIRS)/acute lung injury (ALI) by LPS administration in rats and to measure the content of interleukin-10 massage RNA(IL-10 mRNA) and activator protein-1 (AP-1) activity in order to investigate the anti-inflammatory mechanism.METHODS: Wistar rats were injured with increased dose of LPS to set up the SIRS/ALI model. Reverse transcriptase-polymerase chain reaction(RT-PCR) and electrophoretic mobility shift assays (EMSAs) were used to measure IL-10 mRNA content and the AP-1 binding activity in rat lung, respectively.RESULTS: ①LPS could be applied to simulate SIRS-ALI in rats.②Acute respiratory distress syndrome (ARDS) could be induced under condition of LPS≥6 mg/kg, which was similar to that of the excessive expression of SIRS. ③ LPS may cause the increase content of IL-10 mRNA and AP-1 activity in lung in rat. ④Content of IL-10 mRNA and AP-1 activity were increased significantly under LPS≥6 mg/kg. CONCLUSIONS: ①LPS≥6 mg/kg might cause the SIRS/acute lung injury in rats.②The rats with excessive SIRS/acute lung injury had an obvious increase of transcription of IL-10 gene and upregulated AP-1. ③ Intensified anti-inflammatory mechanism plays a pathological role in SIRS/acute lung injury.

OBJECTIVETo observe the change in IL-13 mRNA expression in rat lungs with acute lung injury (ALI) induced by lipopolysaccharide (LPS), so as to investigate the significance of anti-inflammatory mechanism in the development of ALI.

METHODS(1) Different doses (2 approximately 8 mg/kg) of LPS were injected via the tail vein to the rats to establish ALI model. (2) The IL-13 mRNA content in pulmonary tissue was determined by RT-PCR.

RESULTS(1) Different degrees of ALI was induced in the rats by different doses of LPS. ARDS was produced in the rats by LPS of 6 mg/kg. (2) The IL-13 mRNA expression in the pulmonary tissue could be enhanced by the induction of LPS, especially when its dose was larger than 6 mg/kg.

CONCLUSION(1) Rat ALI model could be produced by LPS injection via the tail vein. (2) LPS in dose of 6 mg/kg was the threshold for the production of rat ARDS. (3) The incidence of rat ARDS might be closely related to the enhanced expression of IL-13 mRNA in rat pulmonary tissue.

Acute Disease ; Animals ; Disease Models, Animal ; Female ; Interleukin-13 ; biosynthesis ; genetics ; Lipopolysaccharides ; Male ; RNA, Messenger ; biosynthesis ; Rats ; Rats, Wistar ; Respiratory Function Tests ; Respiratory Insufficiency ; chemically induced ; metabolism ; physiopathology