The organ chip model is a promising in vitro method for disease modeling that overcomes limitations of traditional experiments lacking cell and tissue interactions and species differences. Lung chips, proposed by Inberg in 2010 (insert literature), have been utilized successfully to simulate lung-related diseases (insert literature). Recently, Qin Jianhua’s team (insert literature) constructed an in vitro lung injury model of COVID-19 using a lung organ chip that replicated the process of vascular barrier damage and immune cell recruitment after virus infection. This model also verified the antiviral effect of remdesivir and its ability to reduce pulmonary vascular barrier damage caused by the virus, offering a new platform for COVID-19 drug screening. Our research team developed a high-throughput lung organ chip and constructed a smoke inhalation lung injury model based on this chip, reproducing alveolar vascular barrier damage due to smoke exposure. We observed oxidative stress, apoptosis, and inflammatory cell infiltration while exploring potential mechanisms through biochemical and protein mass spectrometry techniques. Through our findings, we identified iron death as existing in smoke inhalation lung injury for the first time through chip analysis. Furthermore, we verified that glucocorticoids administered via the airway or intravenous vitamin C can alleviate oxidative stress damage caused by SI-ALI. To our knowledge, this is the first report employing organoid chip technology to model smoke inhalation lung injury, providing new insights into disease mechanism research and drug development.
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