Respiratory

Figure 1: Evaluation of LPS-Induced Acute Lung Injury (ALI) Model. The data are expressed as mean±SEM. **p < 0.01; ***p < 0.001.

Dexamethasone can effectively reduce the secretion of inflammatory factors caused by acute lung injury.

Figure 2: Effects of Dexamethasone (DXMS) treatment on body weight and inflammatory cytokine levels  in the ALI model in BALB/c mice. The data are expressed as mean±SEM. *p < 0.05; **p < 0.01; ***p < 0.001.

Figure 3: Evaluation of Bleomycin (BLM)-Induced Pulmonary Fibrosis Model in C57BL/6 Mice. The data are expressed as mean±SEM. *p < 0.05; **p < 0.01; ***p < 0.001.

Figure 4: Pirfenidone (PFD) ameliorates bleomycin (BLM)-induced pulmonary fibrosis and lung function decline in mice.

Representative histopathological images of lung sections from the experimental groups. Left panels: Hematoxylin and Eosin (H&E) staining evaluating structural destruction, alveolar wall thickening, and inflammatory infiltration. Middle panels: Masson's trichrome staining assessing extracellular matrix accumulation, with blue areas indicating collagen deposition. Right panels: Immunohistochemistry (IHC) staining for α-SMA (brown color). Pulmonary function parameters measured in three groups: G1 (PBS + vehicle control), G2 (BLM + vehicle model), and G3 (BLM + PFD treatment) showed that PFD could significantly improve the lung function of mice. The data is expressed as mean±SEM. *p < 0.05; **p < 0.01; ***p < 0.001.

Figure 5: Evaluation of pulmonary function and lung histopathology at 14 and 21 days post-administration.

Pulmonary function parameters measured at Day 14 and Day 21 post-administration across three experimental groups: G1 (PBS, control), G2 (BLM,PBS), and G3 (BLM,Nerandomilast). Representative microscopic images of lung tissue sections from the respective experimental groups.Left column (H&E): Hematoxylin and Eosin staining evaluating lung structural damage, alveolar wall thickening, and inflammatory cell infiltration.Middle column (Masson): Masson's trichrome staining assessing extracellular matrix accumulation and fibrosis, with collagen deposition stained in blue.Right column (IHC): Immunohistochemical staining for α-SMA  indicated by the brown positive areas. The data are expressed as mean±SEM. * p < 0.05;** p < 0.01; *** p < 0.001.

Figure 6: Establishment and pathophysiological characterization of a cigarette smoke and LPS-induced COPD mouse model.

Experimental Design: Schematic timeline of the modeling protocol. Mice received intratracheal (i.t.) instillation of lipopolysaccharide (LPS) on days 0 and 14, combined with whole-body cigarette smoke exposure from day 1 to 90. At the experimental endpoint, blood, bronchoalveolar lavage fluid (BALF), and lung tissues were collected for downstream analysis, alongside in vivo pulmonary function testing. The data are expressed as mean±SEM. * p < 0.05;** p < 0.01; *** p < 0.001.

Figure 7: Establishment and evaluation of a house dust mite (HDM)-induced acute exacerbation in a cigarette smoke and LPS-induced COPD mouse model.

Schematic representation of the experimental protocol. The COPD mouse model was established via intratracheal (i.t.) instillation of LPS on days 0 and 14, combined with continuous cigarette smoke exposure from days 1 to 90. Subsequently, mice were subjected to HDM induction to simulate an acute exacerbation or asthma-COPD overlap.Total white blood cell (WBC) counts in the bronchoalveolar lavage fluid (BALF) of the COPD, PBS control group (G1) and the COPD, HDM exacerbated group (G2). Relative mRNA expression levels of inflammatory cytokines (IL-2, IL-4, IL-5, IL-6, IL-13) and the mucin gene Muc5ac in lung tissues, comparing G1 and G2. Protein concentrations (pg/mL) of key inflammatory markers (TNF-α, IL-4, IL-5, IL-6, IL-10, IL-13) measured in the COPD, PBS and COPD, HDM groups.Representative histopathological images of lung tissue sections from the respective groups. Top row: Hematoxylin and Eosin (H&E) staining showing structural alterations and inflammatory cell infiltration around the airways. Bottom row: Periodic acid–Schiff (PAS) staining evaluating mucus production. Black arrows indicate distinct goblet cell hyperplasia and profound intra-airway mucus accumulation in the HDM-exposed group compared to the PBS control. The data is expressed as mean±SEM. * p < 0.05;** p < 0.01; *** p < 0.001.

Figure 8: Dose-dependent effects of porcine pancreatic elastase (PPE) on body weight, pulmonary function, inflammation, and lung histopathology in C57BL/6JGpt mice.

Body weight changes (g) monitored over 25 days post-treatment. Mice were treated with either a PBS vehicle (G1), 0.5 U/mouse of PPE (G2), or 1.0 U/mouse of PPE (G3). Evaluation of pulmonary function parameters across experimental groups. Protein concentrations (pg/mL) of key inflammatory cytokines (mTNF-α, mIL-4, mIL-5, mIL-6, mIL-10, and mIL-13) in the BALF. Representative photomicrographs of lung tissues. Left column: H&E staining illustrating dose-dependent alveolar space enlargement and destruction of the alveolar walls typical of emphysematous changes. Right column: Periodic acid–Schiff (PAS) staining highlighting mucus-secreting goblet cells (magenta/purple color) in the airway epithelium.Quantitative morphometric analysis of the histological sections. The top bar graph represents the Mean Linear Intercept (Lm) in micrometers (μm), indicative of the average alveolar diameter and extent of emphysema. The bottom violin plot quantifies the PAS-positive staining area (%). The data is expressed as mean±SEM. 

Figure 9: Establishment and characterization of a Pseudomonas aeruginosa (PA)-induced pneumonia mouse model. Data is expressed as mean±SEM.

Figure 10: Establishment and histopathological characterization of a long-term LPS-induced murine model of chronic nasal inflammation.

Schematic representation of the experimental protocol. Male C57BL/6JGpt mice (8-10 weeks old) were subjected to intranasal instillation of lipopolysaccharide (LPS) three times a week. Body weight was monitored continuously, and biological samples (serum, nasal lavage fluid, and nasal tissues) were collected at specified longitudinal endpoints up to Day 84. Monitoring of body weight over the 84-day treatment period. The graphs display the absolute body weight in grams (top) and the percentage of body weight change (bottom) for the control group (black line) and the LPS-treated group (teal line). Quantitative temporal analysis of nasal mucosal pathology. Line graphs illustrate the dynamic changes in the Hematoxylin and Eosin (HE) inflammatory score, Masson's trichrome positive area (evaluating fibrosis), and Periodic acid–Schiff (PAS) positive area (evaluating mucus production) over the course of the experiment. The data is expressed as mean±SEM.

Figure 11: Evaluation of local inflammatory cell infiltration.

Left graphs: Time-course quantification of total leukocytes, neutrophils, and macrophages in the nasal tissue of control (G1) and LPS (G2) mice. Right panels: Representative immunohistochemistry (IHC) images at D84 showing profound accumulation of CD45+ cells (total leukocytes) and specific neutrophil infiltration in the LPS group. Red arrows point to positively stained cells. The data is expressed as mean±SEM.

Figure 12: Longitudinal profiling of inflammatory cytokines and chemokines.

Line graphs illustrate the dynamic concentrations (pg/mL) of CXCL1, IL-1β, TNF-α, CXCL2, IL-4, IL-6, IL-17A, IFN-γ, and G-CSF in  Serum and  Nasal Lavage Fluid (NLF) across the designated time points. The black lines represent the control group, while the red lines represent the LPS-induced group. The data is expressed as mean±SEM.

Figure 13: Establishment and longitudinal characterization of a surgically-induced Staphylococcus aureus rhinosinusitis mouse model.

Schematic representation of the experimental design. Male C57BL/6JGpt mice (8-10 weeks old) were subjected to surgical injection of Staphylococcus aureus (S.A.) on Day 0 to induce infection. Longitudinal sample collection, including serum, nasal lavage fluid (NLF), and nasal tissues, was performed at prespecified endpoints (Days 7, 28, 42, 56, and up to Day 84). The inset photograph illustrates representative macroscopic signs of the disease, showing purulent inflammation and lesions on the snout (yellow arrow).Clinical evaluations over the 84-day post-treatment period. The left graph displays the percentage of body weight change, and the right graph shows the macroscopic observational sinusitis scores. Black lines denote the control group, while red lines represent the S.A.-infected model group.Histopathological assessment of nasal inflammation. The line graph tracks the dynamic changes in the histological inflammation score over time. Representative Hematoxylin and Eosin (H&E) stained photomicrographs compare the normal nasal structure of the Sham group with the severe pathology of the S.A.-infected group at Day 7. Evaluation of subepithelial fibrosis and mucus hypersecretion. The line graphs quantify the temporal progression of the fibrosis area (% of region) and Periodic acid–Schiff (PAS) positive area (% of region), both demonstrating a distinct peak around Day 42 (indicated by the vertical yellow arrows). The data is expressed as mean±SEM.

Figure 14: Evaluation of local leukocyte infiltration.

The line graph displays the time-course quantification of total leukocytes (CD45+ cells) in the nasal tissue. The accompanying immunohistochemistry images at Day 7 show profound accumulation of CD45+ cells (brown staining, red arrow) in the S.A. infected group compared to the Sham control. The data is expressed as mean±SEM.

Figure 15: Longitudinal profiling of inflammatory cytokines and chemokines.

Line graphs illustrate the dynamic concentrations (pg/mL) of CXCL1, IL-1β, TNF-α, CXCL2, IL-4, IL-6, IL-17A, IFN-γ, and G-CSF in Serum and Nasal Lavage Fluid (NLF) across the designated time points. The black lines represent the Sham group, and the red lines represent the S.A. infected group. The data is expressed as mean±SEM.