Yeh Chiu-Li, Pai Man-Hui, Shih Yao-Ming, Shih Juey-Ming, Yeh Sung-Ling
Department of Nutrition and Health Sciences, Chinese Culture University, Taipei 11114, Taiwan.
School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 11031, Taiwan.
Nutrients. 2017 May 17;9(5):507. doi: 10.3390/nu9050507.
This study investigated the influence of intravenous arginine (Arg) administration on alteration of circulating proangiogenic cells and remote lung injury in a model of polymicrobial sepsis. Mice were assigned to one normal control group (NC) and two sepsis groups that were induced by cecal ligation and puncture (CLP). One of the sepsis groups was injected with saline (SS), whereas the other (SA) was administered with a single bolus of 300 mg Arg/kg body weight via the tail vein 1 h after CLP. Septic mice were sacrificed at either 24 or 48 h after CLP, with their blood and lung tissues collected for analysis. Results showed that septic groups had higher proangiogenic cells releasing factors and proangiogenic cells percentage in blood. Also, concentration of inflammatory cytokines and expression of angiopoietin (Angpt)/Tie-2 genes in lung tissues were upregulated. Arg administration promoted mobilization of circulating proangiogenic cells while it downregulated the production of inflammatory cytokines and expression of Angpt/Tie-2 genes in the lung. The results of this investigation suggested that intravenous administration of Arg shortly after the onset of sepsis enhanced the mobilization of circulating proangiogenic cells, maintained the homeostasis of the Angpt/Tie-2 axis, and attenuated remote organ injury in polymicrobial sepsis.
本研究在多微生物脓毒症模型中,探讨了静脉注射精氨酸(Arg)对循环促血管生成细胞改变及远隔肺损伤的影响。将小鼠分为一个正常对照组(NC)和两个通过盲肠结扎和穿刺(CLP)诱导的脓毒症组。其中一个脓毒症组注射生理盐水(SS),而另一个(SA)在CLP后1小时通过尾静脉给予单次剂量300mg/kg体重的Arg。脓毒症小鼠在CLP后24小时或48小时处死,收集其血液和肺组织进行分析。结果显示,脓毒症组血液中促血管生成细胞释放因子和促血管生成细胞百分比更高。此外,肺组织中炎性细胞因子浓度及血管生成素(Angpt)/Tie-2基因表达上调。给予Arg促进了循环促血管生成细胞的动员,同时下调了肺组织中炎性细胞因子的产生及Angpt/Tie-2基因的表达。本研究结果表明,在脓毒症发作后不久静脉注射Arg可增强循环促血管生成细胞的动员,维持Angpt/Tie-2轴的稳态,并减轻多微生物脓毒症中的远隔器官损伤。