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

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        Shamsaldeen_et_al_311018_accepted_Manuscript.pdf (PDF, 2Mb)
        Author
        Shamsaldeen, Yousif
        Alsugoor, Mahdi
        Lione, Lisa
        Benham, Christopher
        Attention
        2299/21732
        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.
        Publication date
        2019-01-05
        Published in
        European Journal of Pharmacology
        Published version
        https://doi.org/10.1016/j.ejphar.2018.10.056
        Other links
        http://hdl.handle.net/2299/21732
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