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美国学者最近报道了肠内给予精氨酸和谷氨酰胺对肠缺血-再灌注损伤时早期致炎因子的影响。研究人员将肠系膜上动脉夹闭60min后松夹6h,在夹闭后立即向空肠袋内注满精氨酸或谷氨酰胺(60mmol/L),并设对照。应用电泳法对空肠组织核转录因子-κB(NF-κB)以及激活蛋白-1(AP-1)进行分析,并检测AP-1家族中c-jun和c-fos的基因表达。结果显示,NF-κB和AP-1在肠缺血-再灌注过程中均被活化。给予精氨酸的动物AP-1表达显著高于给予谷氨酰胺者,但NF-κB在两组间差异无显著性。研究者认为:精氨酸能增加促炎转录因子AP-1的表达,而不能增加NF-κB的表达,提示精氨酸可能通过一种未知的机制对危重症患者造成损害。浦践一,编译自《JTrauma》,2005,58:455-461;胡森,审校
American scholars recently reported the enteral administration of arginine and glutamine on intestinal ischemia-reperfusion injury early proinflammatory cytokines. Researchers will clamp the superior mesenteric artery 60min after 6h loose clamp, immediately after the closure of the jejunum bag filled with arginine or glutamine (60mmol / L), and set the control. The expression of NF-κB and AP-1 in jejunum tissue were analyzed by electrophoresis and the gene expression of c-jun and c-fos in AP-1 family was detected. The results showed that both NF-κB and AP-1 were activated during intestinal ischemia-reperfusion. The expression of AP-1 in arginine-treated animals was significantly higher than that of glutamine, but there was no significant difference in NF-κB between the two groups. The researchers think: arginine can increase the expression of pro-inflammatory transcription factor AP-1, but can not increase the expression of NF-κB, suggesting that arginine may cause damage to critically ill patients through an unknown mechanism. Pu Jianyi, compiled from “JTrauma”, 2005,58: 455-461; Hu Sen, revision