Fig 2: PI3K‐AKT and HIF‐1 pathway‐related readouts in representative tissue following Galectin‐3 adsorption. (A)–(D) qRT‐PCR quantification of PI3K (A), AKT2 (B), HIF1A (C), and VEGFA (D) mRNA expression measured 3 h after LPS challenge in baseline, sham, and treatment groups (n = 5 per group). Gene expression was normalized to GAPDH and calculated using the 2−ΔΔCt method, expressed as fold change relative to baseline. (E) Representative IHC images from lung tissue (shown as a representative organ) stained for PI3K, AKT, and HIF‐1α across baseline, sham, and treatment groups, with corresponding higher‐magnification insets. (F)–(H) Quantification of the proportion of PI3K‐positive (F), AKT‐positive (G), and HIF‐1α‐positive (H) staining in lung sections (n = 5 per group). Scale bars: 50 µm (main images) and 20 µm (magnified insets). Primary antibodies for IHC were PI3K (Proteintech, 60225‐1‐Ig; 1:400), AKT (Proteintech, 66444‐1‐Ig; 1:400), and HIF‐1α (Bioss, Bs‐0737R; 1:500). Secondary antibodies were goat anti‐mouse IgG (Abcam, ab6789; 1:1000) for PI3K and AKT, and goat anti‐rabbit IgG (Abcam, ab205718; 1:2000) for HIF‐1α. Data are presented as individual values with bars indicating mean ± SEM. Prespecified pairwise comparisons were performed using two‐tailed Mann–Whitney U tests.*p < 0.05, **p < 0.01, ***p < 0.001.