實驗觀察給與敗血症小鼠麩醯胺補充後對其肝臟發炎狀態及氧化壓力的影響。C57BL/6小鼠分為正常控制組(normal control, NC)及敗血症(sepsis)組。敗血症利用盲腸結紮並穿刺手術(cecal ligation and puncture，CLP)引致。CLP後1小時利用尾靜脈注射生理食鹽水(sepsissaline, SS)或麩醯胺溶液(sepsis glutamine , SG)。麩醯胺給與劑量為0.75 g GLN/kg體重。敗血症後24及48小時將老鼠犧牲，取肝臟分析。結果顯示，與控制組相較，肝臟中interleukin (IL) -1, IL-6及tumor necrosis factor (TNF) -α的濃度在敗血症發生後24或48小時顯著增加，而IL-10及transforming growth factor (TGF) -β濃度則降低。CLP後肝臟骨髓過氧化酵素(myeloperoxidase, MPO)活性及脂質過氧化物丙二醛(malondialdehyde, MDA)皆比控制組高。與SS組相較，SG組在敗血症發生後24小時肝臟中IL-6濃度明顯較低， 並在敗血症後的小時明顯減少IL-1、IL-6及TNF-α的表現。CLP後48小時SG組老鼠肝臟中IL-10及TGF-β濃度高於SS組。敗血症發生後24及48小時，SG組老鼠肝臟MPO活性及MDA濃度比SS組低。根據結果顯示，敗血症發生後給予老鼠尾靜脈注射GLN，可以減少肝臟發炎反應及氧化壓力。
This study investigated the effect of intravenous glutamine (GLN) supplementation on the liver's inflammatory response and oxidative stress in a mouse model of polymicrobial sepsis. Mice were randomly assigned to a normal control (NC) group and two sepsis groups. Sepsis was induced by cecal ligation and puncture (CLP). One hour after CLP, septic mice were given saline (SS) or 0.75 g GLN/kg of body weight (SG) once via a tail vein. Septic mice were sacrificed at 24 or 48 h after CLP, and the livers were harvested for further analysis. Results showed that sepsis resulted in higher myeloperoxidase (MPO) activity and malondialdehyde (MDA) production. Interleukin (IU-1, IL-6, and tumor necrosis factor (TNF)-α levels in the liver were upregulated, whereas IL-10 and transforming growth factor (TGF)-β had decreased at 24 and/or 48 h after CLP. Compared to the SS group, the SG group had lower concentrations of IL-1, IL-6, and TNF-α and higher IL-10 and TGF-β levels. Also, MPO activity and MDA concentrations were reduced in liver tissues. These results suggest that sepsis results in inflammation of liver tissues. A single dose of intravenous GLN administration after CLP reduced oxidative stress and attenuated the inflammatory response in livers of mice with polymicrobial sepsis.
