Glucocorticoid receptorβ isoform exhibits a disproportionate increase over the α isoform in the lungs of a polytrauma rat model.

Glucocorticoids (GCs) are potent anti-inflammatory agents that act by binding to the glucocorticoid receptor (GR). GR has two main isoforms, GRα and GRβ, and the balance between GRα and GRβ servesan important role in glucocorticoid sensitivity. In the present study, GRα and GRβ mRNA expression was investigated in the lungs ofa polytrauma rat model. A total of 30 Sprague-Dawley rats were subjected to experimental polytrauma. Animals were sacrificed at 6, 24, and 72 h postoperatively (n=5), and lung tissue and blood samples were collected for analysis. The serum concentrations of tumor necrosis factor α (TNF-α), interleukin (IL)1β, and IL-6 were measured using ELISA kits. The left lobe of the lung was stained with hematoxylin and eosin, and lung myeloperoxidase activity was measured with a myeloperoxidase assay kit. Expression levels of GRα and GRβ mRNA were examined by quantitative polymerase chain reaction. The results revealed a pro-inflammatory response and acute lung injury in this model, and that there was a disproportionate increase in GRβ over GRα in the lung subsequent to polytrauma. The disproportionate increase in GRβ over GRα in the lung after polytrauma may be of crucial importance for the outcome of GC treatment, and adds further evidence to the importance of timing in GC treatment.