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

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Dysfunction in nitric oxide synthesis in streptozotocin treated rat aorta and role of methylglyoxal. / Shamsaldeen, Yousif; Alsugoor, Mahdi; Lione, Lisa; Benham, Christopher.

In: European Journal of Pharmacology, Vol. 842, EJP-48005R3, 05.01.2019, p. 321-328.

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@article{12ddda65a4bc4d209b8e640f22c1594d,
title = "Dysfunction in nitric oxide synthesis in streptozotocin treated rat aorta and role of methylglyoxal",
abstract = "Diabetic vascular dysfunction is a major complication of diabetes. Methylglyoxal (MGO) is a dicarbonyl metabolite elevated in diabetic plasma that reacts with interstitial molecules to form advanced glycation end products (AGE). We investigated whether MGO affects the release of nitric oxide (NO) from rat aortic smooth muscle cells (ASMCs), and if L-arginine can prevent these effects of MGO. MGO was significantly elevated in serum from streptozotocin (STZ)-treated rats (121 ± 11.2 µM) compared with vehicle control rats (27.5 ± 9.2 µM). The pathological concentration of MGO (100 μM) was then applied to investigate its effect on inducible nitric oxide synthase (iNOS) expression and NO release on interferon-gamma (IFN-γ) (100 IU/ml) and lipopolysaccharide (LPS) (100 µg/ml)-stimulated control ASMCs. MGO (100 µM) inhibited IFN-γ and LPS-stimulated iNOS expression through inhibiting Akt phosphorylation and inhibition of iNOS expression was prevented by L-arginine (100 µM) co-treatment. These findings show for the first time that MGO inhibits IFN-γ and LPS-stimulated iNOS expression in ASMCs, in addition to inhibiting IFN-γ and LPS-induced Akt phosphorylation. The actions of MGO might contribute to the vascular dysfunction induced by MGO in diabetes.",
keywords = "diabetes",
author = "Yousif Shamsaldeen and Mahdi Alsugoor and Lisa Lione and Christopher Benham",
year = "2019",
month = jan,
day = "5",
doi = "10.1016/j.ejphar.2018.10.056",
language = "English",
volume = "842",
pages = "321--328",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Dysfunction in nitric oxide synthesis in streptozotocin treated rat aorta and role of methylglyoxal

AU - Shamsaldeen, Yousif

AU - Alsugoor, Mahdi

AU - Lione, Lisa

AU - Benham, Christopher

PY - 2019/1/5

Y1 - 2019/1/5

N2 - Diabetic vascular dysfunction is a major complication of diabetes. Methylglyoxal (MGO) is a dicarbonyl metabolite elevated in diabetic plasma that reacts with interstitial molecules to form advanced glycation end products (AGE). We investigated whether MGO affects the release of nitric oxide (NO) from rat aortic smooth muscle cells (ASMCs), and if L-arginine can prevent these effects of MGO. MGO was significantly elevated in serum from streptozotocin (STZ)-treated rats (121 ± 11.2 µM) compared with vehicle control rats (27.5 ± 9.2 µM). The pathological concentration of MGO (100 μM) was then applied to investigate its effect on inducible nitric oxide synthase (iNOS) expression and NO release on interferon-gamma (IFN-γ) (100 IU/ml) and lipopolysaccharide (LPS) (100 µg/ml)-stimulated control ASMCs. MGO (100 µM) inhibited IFN-γ and LPS-stimulated iNOS expression through inhibiting Akt phosphorylation and inhibition of iNOS expression was prevented by L-arginine (100 µM) co-treatment. These findings show for the first time that MGO inhibits IFN-γ and LPS-stimulated iNOS expression in ASMCs, in addition to inhibiting IFN-γ and LPS-induced Akt phosphorylation. The actions of MGO might contribute to the vascular dysfunction induced by MGO in diabetes.

AB - Diabetic vascular dysfunction is a major complication of diabetes. Methylglyoxal (MGO) is a dicarbonyl metabolite elevated in diabetic plasma that reacts with interstitial molecules to form advanced glycation end products (AGE). We investigated whether MGO affects the release of nitric oxide (NO) from rat aortic smooth muscle cells (ASMCs), and if L-arginine can prevent these effects of MGO. MGO was significantly elevated in serum from streptozotocin (STZ)-treated rats (121 ± 11.2 µM) compared with vehicle control rats (27.5 ± 9.2 µM). The pathological concentration of MGO (100 μM) was then applied to investigate its effect on inducible nitric oxide synthase (iNOS) expression and NO release on interferon-gamma (IFN-γ) (100 IU/ml) and lipopolysaccharide (LPS) (100 µg/ml)-stimulated control ASMCs. MGO (100 µM) inhibited IFN-γ and LPS-stimulated iNOS expression through inhibiting Akt phosphorylation and inhibition of iNOS expression was prevented by L-arginine (100 µM) co-treatment. These findings show for the first time that MGO inhibits IFN-γ and LPS-stimulated iNOS expression in ASMCs, in addition to inhibiting IFN-γ and LPS-induced Akt phosphorylation. The actions of MGO might contribute to the vascular dysfunction induced by MGO in diabetes.

KW - diabetes

U2 - 10.1016/j.ejphar.2018.10.056

DO - 10.1016/j.ejphar.2018.10.056

M3 - Article

VL - 842

SP - 321

EP - 328

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

M1 - EJP-48005R3

ER -