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

Nutrients. 2017 May 17;9(5):507. doi: 10.3390/nu9050507.

Abstract

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.

Keywords: Angpt/Tie-2; arginine; lung injury; proangiogenic cells; sepsis.

MeSH terms

  • Angiopoietins / metabolism
  • Animals
  • Arginine / administration & dosage
  • Arginine / therapeutic use*
  • Bacterial Infections / complications
  • Bacterial Infections / drug therapy
  • Bacterial Infections / microbiology*
  • Endothelial Progenitor Cells / drug effects*
  • Endothelial Progenitor Cells / physiology
  • Gene Expression Regulation / drug effects
  • Injections, Intravenous
  • Lung Injury / etiology
  • Lung Injury / prevention & control*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neovascularization, Physiologic / drug effects*
  • Receptor, TIE-2 / genetics
  • Receptor, TIE-2 / metabolism
  • Sepsis / drug therapy*

Substances

  • Angiopoietins
  • Arginine
  • Receptor, TIE-2
  • Tek protein, mouse