Abstract
Oxidative stress caused by the production of reactive oxygen species (ROS) plays a major role in inflammatory processes. We hypothesized that modulation of ROS via quercetin may protect against oxidative stress and inflammation. Thus, this study aimed to investigate the effects of quercetin on oxidative stress and inflammation in lung epithelial A549 cells. The lipopolysaccharide (LPS)-induced elevation of intracellular ROS levels was reduced after quercetin treatment, which also almost completely abolished the mRNA and protein expression of nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) induced by LPS stimulation. In addition, quercetin suppressed the nuclear translocation of nuclear factor kappa B (NF-κB) and reduced levels of inflammatory cytokine tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6, which had increased significantly after LPS exposure. Our data demonstrated that quercetin decreased ROS-induced oxidative stress and inflammation by suppressing NOX2 production.
Highlights
Acute lung injury (ALI) leading to acute respiratory distress syndrome (ARDS) is a severe clinical disease that involves widespread inflammation in the lung tissues and subsequent development of lung dysfunction [1]
To evaluate whether quercetin reduces LPS-induced oxidative stress and inflammation, we first assessed the effect of quercetin on human lung epithelial A549 cell viability
LPS had no effect on reactive oxygen species (ROS) generation at concentrations below 10 μg/mL in A549 cells, while ROS generation was induced by LPS at concentrations of 10–50 μg/mL
Summary
Acute lung injury (ALI) leading to acute respiratory distress syndrome (ARDS) is a severe clinical disease that involves widespread inflammation in the lung tissues and subsequent development of lung dysfunction [1]. ALI is characterized by disruption of the alveolar–capillary interface, neutrophil recruitment to the lung, and release of chemokines and proinflammatory cytokines by immune cells and non-immune cells such as alveolar epithelial cells [2,3]. Inflammation is a host immune response to chemical and physical injury or infection, usually caused by various bacteria. Excessive inflammation can cause uncontrolled production of inflammatory mediators such as cytokines, chemokines, and reactive oxygen species (ROS) and plays a key role in the development of ALI [4]. Excess production of ROS relative to antioxidant defense causes oxidative stress. Several studies have shown that ROS-generating nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are involved in lipopolysaccharide (LPS)-induced lung inflammation; among members of the large NOX family, NOX2 is the major source for inflammation-associated ROS production in lung inflammation [5,6,7]
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