Abstract
Neutrophil activation is associated with the development of organ injury after trauma–hemorrhagic shock. In the present study, ursolic acid inhibited the superoxide anion generation and elastase release in human neutrophils. Administration of ursolic acid attenuated trauma–hemorrhagic shock-induced hepatic and lung injuries in rats. In addition, administration of ursolic acid attenuated the hepatic malondialdehyde levels and reduced the plasma aspartate aminotransferase and alanine aminotransferase levels after trauma–hemorrhagic shock. In conclusion, ursolic acid, a bioactive natural compound, inhibits superoxide anion generation and elastase release in human neutrophils and ameliorates trauma–hemorrhagic shock-induced organ injury in rats.
Highlights
Trauma-hemorrhagic shock is known to be followed by many life-threatening sequelae [1,2]
Trauma-hemorrhagic shock induces the overproduction of proinflammatory mediators, which plays an important role in the process of organ injury [3,4,5]
Our results suggest that ursolic acid reduces the production of superoxide anion and release of elastase in human neutrophils
Summary
Trauma-hemorrhagic shock is known to be followed by many life-threatening sequelae [1,2]. Previous studies suggest that neutrophils are activated after trauma– hemorrhagic shock, and are essential in the development of organ dysfunction [6,7,8]. Neutrophil infiltration is associated with organ injury, including trauma-hemorrhagic shock [1]. A serine protease in chrymotrypsin family, has important role in the progress of various inflammatory diseases [13,14,15]. In this regards, it is essential to reduce neutrophil oxidative stress and elastase level following injury
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