Mechanical ventilation (MV) is a tool used in critical patient care. However, it can trigger inflammatory and oxidative processes capable of causing or aggravating
lung injuries, which is known as
ventilator-induced lung injury (VILI).
Hesperidin is a
flavonoid with
antioxidant and anti-inflammatory properties in various diseases. The role of
hesperidin in the process triggered by MV is poorly studied. Thus, we hypothesize
hesperidin could protect the lung of mice submitted to
mechanical ventilation. For that, we evaluated cell viability and
reactive oxygen species (ROS) formation in macrophages using different
hesperidin concentrations. We observed
hesperidin did not reduce cell viability, however; it attenuated the production of intracellular ROS in cells stimulated with
lipopolysaccharide (LPS). We further evaluated the effects of
hesperidin in vivo in animals submitted to MV. In the bronchoalveolar lavage fluid, there were higher levels of macrophage, lymphocyte and neutrophil counts in animals submitted to MV, indicating an inflammatory process. In the lung tissue, MV induced oxidative damage and increased
myeloperoxidase activity, though the
antioxidant enzyme activity decreased. MV also induced the production of the inflammatory mediators CCL-2, TNF-α and
IL-12. Pretreatment with
hesperidin resulted in less recruitment of inflammatory cells to the airways and less oxidative damage. Also, it reduced the formation of CCL-2 and
IL-12. Our results show pretreatment with
hesperidin can protect the lungs of mice submitted to
mechanical ventilation by modulating the inflammatory response and redox imbalance and may act to prevent MV injury.