Friend or Foe? The Roles of Antioxidants in Acute Lung Injury

Abstract

Acute lung injury (ALI) is an acute hypoxic respiratory insufficiency caused by various intra- and extra-pulmonary injury factors. The oxidative stress caused by excessive reactive oxygen species (ROS) produced in the lungs plays an important role in the pathogenesis of ALI. ROS is a “double-edged sword”, which is widely involved in signal transduction and the life process of cells at a physiological concentration. However, excessive ROS can cause mitochondrial oxidative stress, leading to the occurrence of various diseases. It is well-known that antioxidants can alleviate ALI by scavenging ROS. Nevertheless, more and more studies found that antioxidants have no significant effect on severe organ injury, and may even aggravate organ injury and reduce the survival rate of patients. Our study introduces the application of antioxidants in ALI, and explore the mechanisms of antioxidants failure in various diseases including it.

Green Tea Polyphenol (-)-Epigallocatechin-3-Gallate (EGCG): A Time for a New Player in the Treatment of Respiratory Diseases?

“…In response to lung injury, there are complex interactions between the circulating polymorphonuclears, particularly neutrophils, and the vascular endothelium. Activated neutrophils play a crucial role in overproduction of ROS, as well [ 30 ].…”

“…In response to lung injury, there are complex interactions between the circulating polymorphonuclears, particularly neutrophils, and the vascular endothelium. Activated neutrophils play a crucial role in overproduction of ROS, as well [30]. In A549 cells and human pulmonary alveolar epithelial cells as well as in the lung of mice, TNFα increased expression of ICAM-1 contributing to the recruitment of polymorphonuclears to the inflammatory site; however, pretreatment with EGCG decreased ICAM-1 expression and the counts of neutrophils and eosinophils in the bronchoalveolar lavage fluid (BALF).…”

“…Understanding the fundamental role of inflammation and inflammation-related oxidative stress in the onset and progression of respiratory diseases has led to use of various antioxidants in the treatment [ 19 , 26 , 27 , 29 , 30 , 31 ]. However, the effectiveness of many existing synthetic antioxidants is not sufficient, or their administration is associated with undesirable side effects.…”

STV‐Na attenuates lipopolysaccharide‐induced lung injury in mice via the TLR4/NF‐kB pathway

“…Tissue injury induce neutrophils migration, which are activated and, engaged with alveolar macrophages, platelets and other inflammatory and fixed lung cells, producing a variety of substances that aggravate inflammation 8–10 . Oxidative stress due to inflammation also exacerbates lung injury even further, and there is significant indications that elevated reactive oxygen species (ROS) production in lung endothelial cells leads to lung barrier integrity reduction, induced by factors such as tumor necrosis factor or LPS 11,12 …”

“…[8][9][10] Oxidative stress due to inflammation also exacerbates lung injury even further, and there is significant indications that elevated reactive oxygen species (ROS) production in lung endothelial cells leads to lung barrier integrity reduction, induced by factors such as tumor necrosis factor or LPS. 11,12 Toll-like receptors are a class of 10 closely similar transmembrane receptors, of which TLRs 1, 2, 4, 5 and 6 are situated on the cell membrane, while TLRs 3, 7, 8, and 9 are situated inside the cell. 13 Lipopolysaccharides, a Gram-negative bacterial cell wall portion, contain lipid A, an oligosaccharide "core" that is not repeating, and distal polysaccharides.…”