Fig.3. Reproduction of Smoke-Induced Injury on the Chip.
- 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.
- 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).
- 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.
- 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.
- A TEM image representing mitochondrial(red circles) and endoplasmic
reticulum(blue circles) in both control and smoke-exposed specimens.
- 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.