Lung function improves after delayed treatment with CNP-miR146a following acute lung injury

Acute respiratory distress syndrome (ARDS) is a highly morbid pulmonary disease characterized by hypoxic respiratory failure. Its pathogenesis is characterized by unrestrained oxidative stress and inflammation, with long-term sequelae of pulmonary fibrosis and diminished lung function. Unfortunately, prior therapeutic ARDS trials have failed and therapy is limited to supportive measures. Free radical scavenging cerium oxide nanoparticles (CNP) conjugated to the anti-inflammatory microRNA-146a (miR146a), termed CNPmiR146a, have been shown to prevent acute lung injury in a pre-clinical model. In this study, we evaluated the potential of delayed treatment with CNP-miR146a at three or seven days after injury to rescue the lung from acute injury. We found that intratracheal CNP-miR146a administered three days after injury lowers pulmonary leukocyte infiltration, reduce inflammation and oxidative stress, lower pro-fibrotic gene expression and collagen deposition in the lung, and ultimately improve pulmonary function. (c) 2021 Elsevier Inc. All rights reserved.

Automated summary

Acute respiratory distress syndrome (ARDS) is a severe lung disease characterized by oxidative stress and inflammation. Current treatment options for ARDS are limited, and there is a need for new therapeutic approaches. A study found that cerium oxide nanoparticles (CNP) conjugated with anti-inflammatory microRNA-146a (miR146a), known as CNP-miR146a, can prevent acute lung injury in a pre-clinical model. Furthermore, delayed treatment with CNP-miR146a showed potential in rescuing the lung from acute injury.