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Intravenous Arginine Administration Promotes Proangiogenic Cells Mobilization and Attenuates Lung Injury in Mice with Polymicrobial Sepsis

机译:静脉注射精氨酸管理促进多生脓毒症小鼠促血管生成细胞的动员并减轻肺损伤。

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摘要

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.
机译:这项研究调查了在多菌性败血症模型中静脉注射精氨酸(Arg)对循环中促血管生成细胞的改变和远端肺损伤的影响。将小鼠分为盲肠结扎穿刺(CLP)诱导的一个正常对照组(NC)和两个败血症组。败血症组中的一个注射了盐水(SS),而另一个(SA)则在CLP后1小时通过尾静脉以300 mg Arg / kg体重的单次推注给药。在CLP后24或48 h处死脓毒症小鼠,收集其血液和肺组织进行分析。结果显示败血组血液中的促血管生成细胞释放因子和促血管生成细胞百分比更高。另外,肺组织中炎性细胞因子的浓度和血管生成素(Angpt)/ Tie-2基因的表达也被上调。精氨酸给药促进循环中的血管生成细胞的动员,同时下调肺中炎性细胞因子的产生和Angpt / Tie-2基因的表达。这项研究的结果表明,脓毒症发作后不久静脉内注射Arg可以增强循环性血管生成细胞的动员,维持Angpt / Tie-2轴的稳态,并减轻多发性败血症的远端器官损伤。

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