The Preventive And Therapeutic Effects Of Diallyl Trisulfide On ALI Mice Induced By Lipopolysaccharide And Related Mechanisms

Objective: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) has been defined as acute, progressive, stubborn respiratory failure with refractory hypoxemia induced by different non-cardiogenic predisposing factors, such as sepsis, trauma and shock. These are most likely to result in multiple organ dysfunction syndrome (MODS). ALI/ARDS has been considered as pulmonary component of systemic inflammatory response syndrome (SIRS) and MODS based on the theory that MODS is induced by excessive inflammation. The pathophysiological pathogenesis of ALI and ARDS is similar, but ARDS is the severe endpoint of ALI. No specific therapy can cure ALI/ARDS, although mechanical ventilation and other methods have been conducted. The desease is devastating in clinic patients and the reported mortality for the dissease ranges from 40% to 60%.Sepsis, especially endotoxin released by Gram-negative bacteria, is the main cause of ALI/ARDS. Lipopololysaccharide (LPS), the main outer membrane component of endotoxin of Gram-negative bacteria, is the most common reagent to duplicate ALI/ARDS model which is similar to ALI/ARDS patients induced by severe infection in clinic. Inflammation and related effector cells, such as neutrophil and macrophage is actived by stimulating with LPS. Uncontrolled release of multiple inflammatory mediators and cytokines including TNF-α, IL-1β, IL-6, PAF have been considered to contribute to the injury of microvascular endothelium and alveolar epithelium. As a result, vascular permeability increases which results in the formation of pulmonary edema, hyaline membrane and interstitial fibrosis. Therefore inflammation and related effector cells, inflammatory...