FIGURE 7.

p50-deficient mice display impaired inflammation resolution and diminished COX-2 expression following RvD1 treatment. WT C57BL/6 mice were i.v. administered LPS (1 μg/ml) for 6, 12, 24, 48, and 72 h or the equivalent volume of sterile 0.9% saline as the control group. Lung tissue samples were collected after LPS administration for morphological evaluations, Western blot analyses, and ELISAs. (A) COX-2 protein expression was assessed via Western blot and analyzed via densitometry. Values were compared with β-actin expression. (B–E) Both WT and p50 KO mice were i.v. administered LPS (3 mg/kg) for 24 h, followed by the administration of RvD1 (5 μg/kg) or vehicle for an additional 24 h. After stimulation, right lungs were harvested. (B) The expression of COX-2 and p50 was determined via Western blot. (C) Representative photomicrographs of pulmonary histology, as shown by H&E staining. Original magnification, ×100 (inset, ×400). Black arrows indicate LPS-induced thickening of the alveolar walls and red arrows show neutrophil infiltration. (D and E) The concentrations of PGE₂ and PGD₂ in homogenized lung tissue were measured via ELISA. Data are shown as mean ± SEM, n = 5–6 mice per treatment per group, and are representative of at least three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.