Maresin 1 Ameliorates Lung IschemiaReperfusion Injury by Suppressing Oxidative Stress via Activation of the Nrf-2-Mediated HO-1 Signaling Pathway

Abstract EN

Lung ischemia/reperfusion (I/R) injury occurs in various clinical conditions and heavily damaged lung function.

Oxidative stress reaction and antioxidant enzymes play a pivotal role in the etiopathogenesis of lung I/R injury.

In the current study, we investigated the impact of Maresin 1 on lung I/R injury and explored the possible mechanism involved in this process.

MaR 1 ameliorated I/R-induced lung injury score, wet/dry weight ratio, myeloperoxidase, tumor necrosis factor, bronchoalveolar lavage fluid (BALF) leukocyte count, BALF neutrophil ratio, and pulmonary permeability index levels in lung tissue.

MaR 1 significantly reduced ROS, methane dicarboxylic aldehyde, and 15-F2t-isoprostane generation and restored antioxidative enzyme (superoxide dismutase, glutathione peroxidase, and catalase) activities.

Administration of MaR 1 improved the expression of nuclear Nrf-2 and cytosolic HO-1 in I/R-treated lung tissue.

Furthermore, we also found that the protective effects of MaR 1 on lung tissue injury and oxidative stress were reversed by HO-1 activity inhibitor, Znpp-IX.

Nrf-2 transcription factor inhibitor, brusatol, significantly decreased MaR 1-induced nuclear Nrf-2 and cytosolic HO-1 expression.

In conclusion, these results indicate that MaR 1 protects against lung I/R injury through suppressing oxidative stress.

The mechanism is partially explained by activation of the Nrf-2-mediated HO-1 signaling pathway.