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Chinese Journal of Burns ; (6): 148-150, 2004.
Article in Chinese | WPRIM | ID: wpr-352230

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the changes in plasma level of interleukin-13 (IL-13) and the changes in the pulmonary IL-13 mRNA content and the pulmonary activator protein-1 (AP-1) activity of the rats inflicted with acute lung injury (ALI) induced by lipopolysaccharide (LPS), so as to explore the relationship between IL-13 expression and AP-1 activity.</p><p><b>METHODS</b>One hundred and twenty Wistar rats were employed in the study and were randomly divided into A (2 mg/kg), B (4 mg/kg), C (6 mg/kg) and D (8 mg/kg) groups according to different dosage of LPS administration and a control group (NS group) at each observing time point. The rats were observed at 1, 2, 4 and 6 postburn hours (PBHs) and every 6 rats were deployed in every group and each time points. A model of systemic inflammatory response syndrome-acute lung injury (SIRS-ALI) was replicated in Wistar rats. The plasma content of IL-13 was assayed by enzyme-linked immunosorbent assay (ELISA), and the pulmonary tissue content of IL-13 mRNA and AP-1 activity by reverse transcriptase-polymerase chain reaction (RT-PCR) and electrophoretic mobility shift assays (EMSA).</p><p><b>RESULTS</b>The plasma content of IL-13, pulmonary content of IL-13 mRNA and AP-1 activity increased simultaneously after LPS administration. All the above indices were significantly different statistically between the LPS groups and the control group (P < 0.05 - 0.01). The plasma level of IL-13 and pulmonary tissue mRNA content and AP-1 activity in A, B, C and D groups were increased significantly with peak levels at 2 PBHs.</p><p><b>CONCLUSION</b>The pulmonary AP-1 activity increased with the enhanced expression of IL-13, which was related to the development of SIRS-ALI.</p>


Subject(s)
Animals , Female , Male , Rats , Acute Lung Injury , Metabolism , Endotoxins , Toxicity , Interleukin-13 , Blood , Genetics , Physiology , Lung , Chemistry , Rats, Wistar , Transcription Factor AP-1 , Physiology
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