ABSTRACT
Acute lung injury [ALl] or acute respiratory distress syndrome is a serious clinical problem with high mortality. Oxidative stress was found to play a major role in mediating lung injury and antioxidants have been shown to be effective in attenuating ALI. In this study, we determine the effects of tempol, a membrane-permeable radical scavenger, in lipopolysaccharide [LPS] induced ALl and the underlying mechanism. ALl was induced by intraperitoneal injection of LPS [lmglkg] and mice were treated with tempol 30 mm before injection of LPS. One hour later, bronchoalveolar lavage fluid [BALF] was collected and subjected to estimation of total and differential cell counts as svell as the proinflammatory cytokines; tumor necrosis factor-alpha [TNF-alpha], interleukin-1beta [IL-1beta] and interferon-gamma [IFN-gamma]. Lung tissue damage was confirmed by histopathological changes and by immunohistochemical analysis of myeloperoxidase [MPO]. Moreover, lipid peroxidation, reduced glutathione [GSH] and nitric oxide [NO] were investigated in the lung tissue. Pretreatment with tempol produced significant attenuation of LPS-induced lung injury as well as inhibition of LPS mediated increase in MPO immunostaining, MDA and NO levels in lung tissue. Elevated cytokines levels in both BALF and lung tissue homogenates of ALl mice were significantly decreased after administration of tempol. These findings confirmed significant protection by tempol against LPS-induced acute lung injury and that superoxide anion scavenging appears to be a potential target for new potential therapy in pulmonary disorders