Mitochondrial transplantation attenuates alveolar epithelial cell dysfunction and reduces disruption of tight junction proteins to alleviate lung ischaemia-reperfusion injury

Objective The aim of this study was to investigate the therapeutic effect of exogenous mitochondrial transplantation (MT) on lung ischemia-reperfusion injury (LI/RI) and to investigate the effect of mitochondrial transplantation on alveolar epithelial cell function as well as on the ultrastructural changes of the alveolar epithelial barrier ultrastructural changes. Methods The therapeutic effect of mouse liver-derived mitochondrial transplantation on LI/RI was assessed by constructing a hypoxia-reoxygenation model of mouse alveolar epithelial cells (MLE-12 cells) and a lung ischaemia-reperfusion injury model in C57BL/6 male mice, which simulated the pathological process of LI/RI. Results The study results showed that MT exhibited significant therapeutic potential in LI/RI. In vitro and in vivo experiments revealed that MT significantly improved lung tissue injury by reducing oxidative stress, inflammatory response, apoptosis, and necrosis. Meanwhile, MT could alleviate alveolar epithelial cell dysfunction, reduce the disruption of tight junction proteins, and protect the alveolar epithelial barrier, thereby mitigating LI/RI. Conclusion This study confirmed in a lung ischemia-reperfusion injury model that MT treatment can repair the structural damage of the alveolar barrier caused by ischemia-reperfusion by targeting and regulating the expression of tight junction proteins in alveolar epithelial cells, providing a new perspective for elucidating the functional targets of MT treatment in protecting the alveolar barrier.