Fig. 3
From: Interleukin-3 plays a vital role in hyperoxic acute lung injury in mice via mediating inflammation
Effect of IL-3 on proinflammatory mediators and nuclear factor (NF)-κB activation in mice. Tumor necrosis factor (TNF)-α and interleukin (IL)-6 (a) in bronchoalveolar lavage fluids (BALF), phosphorylated (p)-IκBα in the cytoplasm (b), nuclear factor (NF)-κB p65 in the nucleus (c), p-IκBα kinase (IKK) β (d), and NF-κB activity (e) in lung tissues were assessed 72 hours after hyperoxia or room air challenge by enzyme linked immunosorbent assay (ELISA) or western blotting. Data represent assessments in a minimum of n = 5 mice. *P <0.05 vs. sham+wild type (WT) group; † P <0.05 vs. hyperoxia+WT group. IL-3–/–, IL-3 gene disrupted mice