Abstract
Changes in tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-10 and vascular endothelial growth factor (VEGF) in serum and bronchoalveolar lavage fluid (BALF) in rats with acute respiratory distress syndrome (ARDS) and the intervention effect of dexamethasone were observed to explore the theoretical basis of dexamethasone in the treatment of ARDS. Seventy-two rats were randomly divided into normal control group (group N, n=24), ARDS model group (group L, n=24) and dexamethasone group (group D, n=24). The ARDS rat model was established by jointly injecting oleic acid and lipopolysaccharide via the caudal vein, while rats in group D received intervention with dexamethasone. The wet/dry weight ratios of lung tissues were measured, and the levels of TNF-α, IL-6, IL-10 and VEGF in serum and BALF were measured via enzyme-linked immunosorbent assay. The wet/dry weight ratio of lung tissues of rats in group D was significantly decreased compared with that in group L (P<0.05 or P<0.01). The levels of TNF-α, IL-6 and VEGF in serum and BALF of rats in group L and D were obviously increased compared with those in group N at each time point (P<0.01). The levels of TNF-α, IL-6 and VEGF in serum and BALF of rats in group D were significantly decreased compared with those in group L (P<0.01). In conclusion, there is a serious imbalance between anti-inflammatory response and inflammatory response in rats with ARDS induced by oleic acid combined with lipopolysaccharide of Escherichia coli, whereas dexamethasone can alleviate lung injury through inhibiting expression levels of inflammatory factors and promoting expression levels of anti-inflammatory factors.
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