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Dysfunction in nitric oxide synthesis in streptozotocin treated rat aorta and role of methylglyoxal

Yousif A Shamsaldeen1, Mahdi H Alsugoor2, Lisa A Lione3

  • 1Pharmacology Group, School of Life and Medical Sciences, University of Hertfordshire, College Lane, Hatfield, Hertfordshire AL10 9AB, United Kingdom; Department of Physiology, Pharmacology and Neuroscience, Biomedical Sciences Building, University of Bristol, Bristol BS8 1TD, United Kingdom.

European Journal of Pharmacology
|November 5, 2018
PubMed

Insights

Methylglyoxal (MGO), elevated in diabetes, impairs nitric oxide (NO) release from aortic smooth muscle cells by inhibiting inducible nitric oxide synthase (iNOS) expression. L-arginine prevents these detrimental effects, suggesting a therapeutic target for diabetic vascular dysfunction.

Area of Science:

  • Biochemistry
  • Physiology
  • Endocrinology

Background:

  • Diabetic vascular dysfunction is a significant complication of diabetes.
  • Methylglyoxal (MGO) is a dicarbonyl metabolite elevated in diabetic plasma, contributing to advanced glycation end product (AGE) formation.
  • Nitric oxide (NO) plays a crucial role in vascular health.

Purpose of the Study:

  • To investigate the effect of MGO on nitric oxide (NO) release from rat aortic smooth muscle cells (ASMCs).
  • To determine if L-arginine can prevent MGO-induced alterations in NO release and related molecular pathways.
  • To examine MGO's impact on inducible nitric oxide synthase (iNOS) expression and Akt phosphorylation in ASMCs.

Main Methods:

  • Measurement of MGO levels in serum from streptozotocin (STZ)-induced diabetic rats and control rats.
  • Application of pathological MGO concentrations (100 μM) to ASMCs stimulated with interferon-gamma (IFN-γ) and lipopolysaccharide (LPS).
  • Assessment of iNOS expression, NO release, and Akt phosphorylation in response to MGO and L-arginine co-treatment.

Main Results:

  • MGO levels were significantly elevated in STZ-treated rats compared to controls.
  • MGO (100 μM) inhibited IFN-γ and LPS-stimulated iNOS expression in ASMCs.
  • MGO inhibited IFN-γ and LPS-induced Akt phosphorylation, an effect prevented by L-arginine (100 μM) co-treatment.

Conclusions:

  • Methylglyoxal (MGO) inhibits IFN-γ and LPS-stimulated iNOS expression and Akt phosphorylation in ASMCs.
  • L-arginine co-treatment prevents MGO-induced inhibition of iNOS expression.
  • MGO's inhibitory actions on iNOS may contribute to the vascular dysfunction observed in diabetes.
Keywords:
Diabetes mellitusINOSL-arginineMethylglyoxalNitric oxideVascular dysfunction

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