期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 23, 期 2, 页码 658-663出版社
ELSEVIER
DOI: 10.1016/j.intimp.2014.10.019
关键词
IEX-1; Reactive oxygen species; Mitoquinone; Sepsis
资金
- National Institutes of Health [CA158756, AI089779, DA028378]
Sepsis, a leading cause of mortality in intensive care units worldwide, is often a result of overactive and systemic inflammation following serious infections. We found that mice lacking immediate early responsive gene X-1 (IEX-1) were prone to lipopolysaccharide (LPS) -induced endotoxemia. A nonlethal dose of LPS provoked numerous aberrations in lEX-1 knockout (1(0) mice including pancytopenia, increased serum aspartate aminotransferase (AST), and lung neutrophilia, concurrent with liver and kidney damage, followed by death. Given these results, in conjunction with a proven role for lEX-1 in the regulation of reactive oxygen species (ROS) homeostasis during stress, we pre-treated IEX-1 KO mice with Mitoquinone (MitoQ), a mitochondrion-based antioxidant prior to LPS injection. The treatment significantly reduced ROS formation in circulatory cells and protected against pancytopenia and multiple organ failure, drastically increasing the survival rate of IEX-1 KO mice challenged by this low dose of LPS. This study confirms significant contribution of mitochondrial ROS to the etiology of sepsis. Published by Elsevier B.V.
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