Maresin 1 Attenuates Ventilator-induced Lung Injury by Reducing Oxidative Stress through the Nrf2/HO-1 and NF-κB Pathways

Abstract Mechanical ventilation could support the lives of patients with respiratory failure in a variety of ways, including maintaining airway patency and improving oxygenation, etc. However, mechanical ventilation itself could lead to lung damage, which is called mechanical ventilation-related lung injury (VILI). The incidence of VILI is high and the prognosis is poor, so clarifying the mechanism of VILI and seeking effective preventive and therapeutic measures are the urgent medical problem to be resolved. By constructing the VILI model, we studied the effect of Maresin1 on VILI and explored its possible mechanism at the animal level. We tested the related indicators of lung injury, the oxidative stress response, and the inflammatory response. The results indicated that Maresin1 could inhibit the oxidative stress response and excessive inflammation, thus ameliorating lung injury in VILI. We also detected the expression levels of the principal oxidative stress pathway Nrf2 / HO-1 and the key inflammatory transcription factor NF-κB. We used the HO-1 inhibitor ZnPP to further confirm our conclusion. Our results suggested for the first time that Maresin1 could promote the activation of the Nrf2 / HO-1 pathway and significantly suppress the expression of NF-κB to exert a positive role in VILI.