Glutamine treatment decreases plasma and lymph cytotoxicity during sepsis in rats.
Glutamine (Gln) is considered as a conditionally essential amino acid. Pharmacological supplementation of Gln helps to maintain the intestinal mucosal barrier, modulate cytokine production, and prevent organ injury during sepsis. Our previous study demonstrated the different effects of Gln on macrophage cytokine production in vitro or in vivo. The purpose of this study was to investigate the potential mechanism of Gln treatment to protect cells and modulate inflammation during sepsis in vivo. The results showed that administration of Gln significantly attenuated plasma-induced macrophage cytokine production and endothelial cell necrosis after cecal ligation and puncture in rats. In addition, it preserved human umbilical vein endothelial cell (HUVEC) viability and migration ability. Gln treatment also reduced lymph cytotoxicity by restoring macrophage tumor necrosis factor-α production, maintaining HUVEC viability, and decreasing endothelial cell necrosis. Mesenteric lymph duct ligation did not alleviate plasma cytotoxicity. Plasma lipopolysaccharide and d-lactate levels were suppressed after Gln treatment. Taken together, these results indicated that Gln administration can protect cells by attenuating the cytotoxicity of plasma and mesenteric lymph during sepsis.
Department of Anesthesiology/Intensive Care Unit,  Shanghai Sixth People's Hospital,  Medical College of Shanghai Jiaotong University, Shanghai 200233,  China.
Xuemin
X
Wang
Ying
Y
Xue
Menfan
M
Liang
Wei
W
Jiang
D000818:Animals; D001769:Blood / Q000378:metabolism; D015153:Blotting, Western; D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004797:Enzyme-Linked Immunosorbent Assay; D005973:Glutamine / Q000097:blood / Q000494:pharmacology*; D050884:HSP72 Heat-Shock Proteins / Q000378:metabolism; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D019344:Lactic Acid / Q000097:blood; D008070:Lipopolysaccharides / Q000097:blood; D008196:Lymph / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008643:Mesentery / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000097:blood / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D050884:HSP72 Heat-Shock Proteins; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D005973:Glutamine; D019344:Lactic Acid