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Chrysin and Luteolin Attenuate Diabetes‐Induced Impairment in Endothelial‐Dependent Relaxation: Effect on Lipid Profile, AGEs and NO Generation
Author(s) -
ElBassossy Hany M.,
AboWarda Shaymaa M.,
Fahmy Ahmed
Publication year - 2013
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.4917
Subject(s) - chrysin , endocrinology , medicine , luteolin , diabetes mellitus , streptozotocin , cholesterol , dyslipidemia , phenylephrine , endothelial dysfunction , chemistry , quercetin , blood pressure , flavonoid , biochemistry , antioxidant
Chrysin and luteolin are two important plant flavonoids. In the present study, we hypothesized that they protect against deleterious vascular effects of diabetes. Diabetes was induced in rats by streptozotocin (STZ) injection, while chrysin and luteolin were administered two weeks after STZ administration for 6 weeks. Then, blood pressure (BP) and serum levels of glucose, advanced glycation end products (AGEs), triglycerides (TGs), total cholesterol and low density lipoprotein–cholesterol (LDL‐C) were determined. Concentration response curves for KCl, phenylephrine (PE), acetylcholine (ACh) and ACh‐induced NO generation were obtained in isolated aorta. Compared with control, diabetes increased diastolic and systolic BP, while chrysin and luteolin attenuated diastolic BP elevation without affecting the developed hyperglycemia. Diabetes increased contractile response of aorta to KCl, PE, decreased relaxation response to ACh, while chrysin and luteolin prevented the impaired response to ACh. In addition, diabetes was accompanied by elevated levels of TGs, total and LDL cholesterol, while both chrysin and luteolin prevented this dyslipidemia. Furthermore, chrysin decreased the elevated AGEs level in serum of diabetic animals, while luteolin abrogated the impaired NO generation in diabetic aorta. Collectively, chrysin and luteolin attenuate diabetes‐evoked impairment in endothelial‐dependent relaxation possibly via ameliorating detrimental changes in lipid profile, AGEs and NO generation. Copyright © 2013 John Wiley & Sons, Ltd.