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Carnosine Supplementation Enhances Post Ischemic Hind Limb Revascularization.

Adjoa A Boakye1, Deqing Zhang1,2, Luping Guo1,2

  • 1Diabetes and Obesity Center, University of Louisville, Louisville, KY, United States.

Frontiers in Physiology
|July 18, 2019
PubMed
Summary

Carnosine supplementation improved blood flow and limb function after ischemia in mice. This suggests carnosine enhances healing by boosting angiogenic signaling, potentially through iron chelation.

Keywords:
Flk-1+/Sca-1+ cells4-hydroxy-nonenalHIF-1αangiogenesishind limb ischemiairon chelationperipheral arterial diseaseprolyl hydroxylases

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Area of Science:

  • Biochemistry
  • Physiology
  • Molecular Biology

Background:

  • Skeletal muscle contains high concentrations of the histidine dipeptide carnosine.
  • Carnosine's known functions include buffering pH, chelating metals, and scavenging free radicals.
  • Its precise role in protecting against tissue injury, particularly post-ischemia, requires further elucidation.

Purpose of the Study:

  • To investigate if carnosine protects against post-ischemic injury by enhancing hypoxia-inducible factor 1-alpha (HIF-1α) angiogenic signaling through iron (Fe2+) chelation.
  • To evaluate the therapeutic potential of carnosine in improving recovery from hind limb ischemia (HLI).

Main Methods:

  • Wild type C57BL/6 mice were subjected to HLI and supplemented with carnosine.
  • Blood flow, limb function, revascularization, and myocyte regeneration were assessed.
  • Expression of HIF-1α, vascular endothelial growth factor (VEGF), and related markers was analyzed in ischemic tissues and cells.
  • Experiments included in vitro studies with C2C12 myoblast cells and in vivo studies with carnosine analogs.

Main Results:

  • Carnosine supplementation in HLI mice led to improved blood flow recovery, enhanced limb function, and better revascularization and myocyte regeneration compared to controls.
  • Increased carnosine bioavailability in ischemic limbs correlated with enhanced proton-coupled oligopeptide transporter expression.
  • Carnosine treatment upregulated HIF-1α and VEGF expression in ischemic tissues and increased circulating proangiogenic Flk-1+/Sca-1+ cells.
  • In vitro, carnosine and octyl-D-carnosine boosted HIF-1α and VEGF levels in hypoxic myoblasts.
  • A carnosine analog lacking Fe2+ chelating capacity (methylcarcinine) did not affect HIF-1α or VEGF levels, suggesting the importance of iron chelation.

Conclusions:

  • Carnosine promotes post-ischemic revascularization and tissue repair.
  • The mechanism involves augmenting pro-angiogenic HIF-1α/VEGF signaling.
  • Fe2+ chelation by carnosine appears to be a key factor in this process.