Abstract
To assess the effect of taurine on lipopolysaccharide (LPS)-induced lung inflammation, oxidative stress and apoptosis, female Golden Syrian hamsters were intratracheally instilled with bacterial LPS (0.02 mg in phosphate buffered saline (PBS) pH 7.4), before or after a 3-day intraperitoneal treatment with a single dose of taurine (50 mg/kg/day in PBS pH 7.4), and bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected at 24 hr after the last treatment. In comparison to BALF samples from animals receiving only PBS pH 7.4, and serving as controls, those of LPS-stimulated animals exhibited a higher count of both total leukocytes and neutrophils and increased expression of tumor necrosis factor receptor 1. In comparison to lungs from control animals, those from LPS-treated animals showed increased cellular apoptosis, lipid peroxidation, decreased glutathione levels, altered activities of antioxidant enzymes (catalase, glutathione peroxidase, superoxide dismutase) and focal inflammation confined to the parenchyma. A treatment with taurine was found to significantly attenuate all these alterations, with the protection being, in all instances, greater when given before rather than after LPS. The present results suggest that taurine is endowed with antiinflammatory and antioxidant properties that are protective in the lung against the deleterious actions of Gram negative bacterial endotoxin.
Highlights
Acute lung injury (ALI) is a characteristic sequel to infection by Gram negative bacteria and an important cause of morbidity and mortality in humans [1]
The relevance of oxidative stress to the development of ALI is supported by the results of studies in experimental animal models of ALI demonstrating that low molecular weight antioxidant compounds possessing a wide range of structural features and biological activities are able to decrease the severity of the inflammatory process by reducing the migration of macrophages, monocytes and neutrophils into the lung [23] and the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) by these cells [24,25]
An earlier study from this laboratory determined that a 3-day treatment of hamsters with TAU was able to reduce the number of proinflammatory leukocytes, the expression of tumor necrosis factor receptor 1 (TNFR1) on macrophages, the activation of caspase-3 activity and accompanying apoptosis, lipid peroxidation (LPO) and the decreases in reduced glutathione (GSH) and activities of antioxidant enzymes in bronchoalveolar lavage fluid (BALF) samples as a result of a challenge with LPS [31]
Summary
Acute lung injury (ALI) is a characteristic sequel to infection by Gram negative bacteria and an important cause of morbidity and mortality in humans [1]. An earlier study from this laboratory determined that a 3-day treatment of hamsters with TAU was able to reduce the number of proinflammatory leukocytes, the expression of tumor necrosis factor receptor 1 (TNFR1) on macrophages, the activation of caspase-3 activity and accompanying apoptosis, LPO and the decreases in GSH and activities of antioxidant enzymes in bronchoalveolar lavage fluid (BALF) samples as a result of a challenge with LPS [31]. On the basis of these results, the present study was undertaken in hamsters with the specific purpose of determining: (a) the effects of TAU on the inflammation, oxidative stress and apoptosis that develops in lung tissue as a result of an exposure to LPS, (b) the role of the order of administration of TAU relative to that of LPS on the magnitude of the effects demonstrated by TAU, and (c) the extent to which the findings for lung tissue samples correlate with those gathered for markers of inflammation in BALF samples
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