Antiglycation Activities and Common Mechanisms Mediating Vasculoprotective Effect of Quercetin and Chrysin in Metabolic Syndrome. (27th July 2020)

• Record Type: Journal Article
• Authors: Ahmed, Osama A. A.; Azhar, Ahmad S.; Tarkhan, Mayada M.; Balamash, Khadijah S.; El-Bassossy, Hany M.
• Other Names: Rahman Khalid Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2020(2020)
• Publication Date: 2020-07-27
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2020/3439624
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : Multiple risk factors combine to increase the risk of vascular dysfunction in patients suffering from metabolic syndrome (MetS). The current study investigates the extent to which quercetin (Q) and chrysin (CH) protect against vascular dysfunction in MetS rats. MetS was induced by feeding rats a high-salt diet (3%) and fructose-enriched water (10%) for 12 weeks. Thoracic aorta was isolated from MetS rats and from control rats, with the latter being injured by methylglyoxal (MG). Aortae were incubated with CH and Q, and vascular reactivity was evaluated through the analysis of aortic contraction and relaxation in response to PE and ACh, respectively. The formation of advanced glycation end products (AGEs) and the free radical scavenging activity of 1, 1-diphenyl-2-picrylhydrazyl (DPPH) were also evaluated following the introduction of CH and Q. The increased vasoconstriction and impaired vasodilation in MetS aortae were significantly ameliorated by Q and CH. Similarly, they ameliorated glycation-associated exaggerated vasoconstriction and impaired vasodilation produced by MG in control aortae. In addition, both Q and CH were effective in reducing the formation of AGEs and inhibition of glycosylation in response to MG or fructose treatment. Finally, Q successfully scavenged DPPH free radicals while CH showed significant vasodilation of precontracted aorta that was inhibited by L-NAME. In conclusion, Q and CH provide protection against vascular dysfunction in MetS by interfering with AGEs formations and AGEs-associated vascular deterioration, with CH being largely dependent on NO-mediated mechanisms of vasodilation.