Fig.3. Reproduction of Smoke-Induced Injury on the Chip.
  1. Immunofluorescence images depicting apoptosis (Annexin V-FITC stained) across control and smoke-exposed groups, together with a statistical comparison. Data from three independent studies are presented as mean ± standard deviation (SD). n=3, scale bars=30 μm.
  2. Detection of FITC-Dextran (40 kDa) translocation from the upper to the lower layer, evidencing alveolar-capillary barrier disruption and quantitative analysis of barrier leakage on the chip by testing fluorescence intensity of FITC-dextran in the alveolar cavity of the chip.it was performed at different time points between the control and smoke-exposed groups (n=6). The results are expressed as mean ± standard deviation (SD).
  3. Assessment of oxidative stress (DHCA-ROS stained) on the chip following smoke exposure, accompanied by a corresponding statistical analysis. The results, derived from three independent trials, are expressed as mean ± standard deviation (SD). n=3, scale bars=30 μm.
  4. Immunofluorescence imaging to reveal the adhesion patterns of THP-1 cells (Calcein AM and PI stained) in control versus smoke-exposed environments, including an analysis of mean optical density for THP-1 cell adhesion. The results are based on three separate experiments and expressed as mean ± standard deviation (SD). n=3, scale bars, 50 μm.
  5. A TEM image representing mitochondrial(red circles) and endoplasmic reticulum(blue circles) in both control and smoke-exposed specimens.
  6. Illustration of the pathogenesis of fire-related smoke-induced acute lung injury (SI-ALI), including alveolar-capillary barrier impairment, oxidative stress, apoptosis, and immune cell adhesion.