AI Article Synopsis
- Long-term cigarette smoke exposure leads to lung damage and inflammation, primarily causing emphysema, a key symptom of chronic obstructive pulmonary disease (COPD).
- Current treatments aim to alleviate symptoms but often fail to resolve inflammation.
- The study investigated the effects of the specialized pro-resolving mediator AT-RvD1 on a mouse model of emphysema, finding improvements in lung structure, reduced inflammation, and decreased oxidative stress through the activation of the Nrf2/Keap1 pathway.
Article Abstract
Long-term exposure to cigarette smoke (CS) results in alveolar parenchyma destruction due to chronic inflammatory response and the imbalance between oxidants and antioxidants, and proteases and antiproteases. Emphysema is the main symptom of chronic obstructive pulmonary disease. Current treatment focuses on relieving respiratory symptoms, and inflammation resolution failure is an important pathophysiological element of the disease. Specialized pro-resolving mediators (SPMs) synthesized endogenously during resolution processes demonstrated beneficial effects in murine models of airway inflammation. Here, we aimed to test the SPM AT-RvD1 in a murine model of CS-induced emphysema. AT-RvD1 restored elastic fibers and lung morphology, with reduction in MMP-3, neutrophils, and myeloperoxidase activity and increases in macrophages and IL-10 levels. AT-RvD1 also decreased levels of oxidative stress markers and ROS via upregulation of the Nrf2/Keap1 pathway. Therefore, we suggest that AT-RvD1 causes pro-resolutive action in our murine model of CS-induced emphysema by upregulation of the Nrf2/Keap1 pathway.
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| http://dx.doi.org/10.1016/j.intimp.2018.01.045 | DOI Listing |
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