CeO2-NPs Attenuates Apoptosis and EMT in Rat Lung Exposed to Hyperoxia by Inhibiting M1 Macrophage Polarization

Abstract

Oxygen therapy is widely used therapeutically in the treatment of acute and chronic hypoxemia. However, hyperoxia—elevated inhaled oxygen—causes hyperoxic acute lung injury (HALI). HALI is mainly related to excessive production of reactive oxygen species (ROS). Effective treatment strategies for HALI remain limited. Apoptosis and epithelial-to-mesenchymal transition (EMT) are significant signs of lung damage after exposure to hyperoxia. HALI Responds to Inflammatory Response. Suppressing inflammation induced by M1 macrophage polarization. protects against HALI.

CeO₂-NP_S are representative nano-antioxidants. In this study, we clarified the role of CeO₂-NPs in lung tissues of hyperoxia-exposed rats and the effect of CeO₂-NPs on macrophage polarization. CeO₂-NP_S attenuated lung injury induced by hyperoxia exposure. In addition, CeO₂-NP_S reduced the apoptosis, increased the expression of Bcl-2 and decreased expression of Bax and cleaved-caspase 3. CeO₂-NP_S also reduced EMT in the lung of hyperoxia-exposed rats. CeO₂-NP_S reduced the expression of IL-1β, TNF-ɑ, IL-6. Our study showed that hyperoxia promoted M1 macrophage polarization, which was reduced by CeO₂-NP_S treatment.

In conclusion, hyperoxia induced lung injury and promoted apoptosis and EMT in rats, and CeO₂-NP_S had a therapeutic effect on HALI. CeO₂-NP_S reduced the release of inflammatory factors and M1 macrophage polarization in rats following hyperoxia exposure. CeO₂-NPs attenuates apoptosis and EMT in rat lungs exposed to hyperoxia by inhibiting M1 macrophage polarization.