Nutrition (Burbank, Los Angeles County, Calif.) · 2009
Glutamine attenuates lipopolysaccharide-induced acute lung injury.
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Zhang Feng, Wang Xinying, Pan Liya, Wang Weiya, Li Ning, Li Jieshou
Аннотация
OBJECTIVES: It has been reported that glutamine (GLN) can attenuate acute lung injury after sepsis. GLN is also thought to be a precursor of glutathione (GSH) synthesis. Using the GSH synthesis blocker, L-buthionine-(S,R)-sulfoximine (BSO), we investigated the role of GSH synthesis in the protective effect of GLN on acute lung injury.
METHODS: In this study, we used an acute lung injury model induced by intratracheal injection of lipopolysaccharide (1 mg mL(-1) kg(-1)). GLN (0.75 g/kg, intravenous) and BSO (2 mmol/kg, intraperitoneal) were administrated simultaneously. At 2 and 18 h after the injections, the rats were sacrificed by right ventricular puncture and bronchoalveolar lavage was done. The lower right lung was excised for histologic examination. Total protein concentration and total cell and neutrophil counts in the bronchoalveolar lavage fluid were determined. CD11b expression in the blood was determined by flow cytometry. We also analyzed myeloperoxidase activity, and GSH and interleukin-8 levels in lung tissues.
RESULTS: GLN supplementation reduced the total protein concentration and total cell and neutrophils counts in bronchoalveolar lavage fluid after lipopolysaccharide challenge. GLN enhanced GSH synthesis and attenuated interleukin-8 release and myeloperoxidase activity in lung tissues. GLN also decreased CD11b expression in blood neutrophils and prevented lung histologic changes. BSO abolished the effects of GLN and attenuated its protection on acute lung injury.
CONCLUSION: These results indicate that GLN could prevent neutrophil recruitment and infiltration, protect the alveolar barrier, and attenuate inflammatory injury during sepsis. This effect may be related to enhanced GSH synthesis.
METHODS: In this study, we used an acute lung injury model induced by intratracheal injection of lipopolysaccharide (1 mg mL(-1) kg(-1)). GLN (0.75 g/kg, intravenous) and BSO (2 mmol/kg, intraperitoneal) were administrated simultaneously. At 2 and 18 h after the injections, the rats were sacrificed by right ventricular puncture and bronchoalveolar lavage was done. The lower right lung was excised for histologic examination. Total protein concentration and total cell and neutrophil counts in the bronchoalveolar lavage fluid were determined. CD11b expression in the blood was determined by flow cytometry. We also analyzed myeloperoxidase activity, and GSH and interleukin-8 levels in lung tissues.
RESULTS: GLN supplementation reduced the total protein concentration and total cell and neutrophils counts in bronchoalveolar lavage fluid after lipopolysaccharide challenge. GLN enhanced GSH synthesis and attenuated interleukin-8 release and myeloperoxidase activity in lung tissues. GLN also decreased CD11b expression in blood neutrophils and prevented lung histologic changes. BSO abolished the effects of GLN and attenuated its protection on acute lung injury.
CONCLUSION: These results indicate that GLN could prevent neutrophil recruitment and infiltration, protect the alveolar barrier, and attenuate inflammatory injury during sepsis. This effect may be related to enhanced GSH synthesis.