1. Isoliquiritigenin attenuates inflammation and modulates Nrf2/caspase-3 signalling in STZ-induced aortic injury.
- Author
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Alzahrani S, Said E, Ajwah SM, Alsharif SY, El-Bayoumi KS, Zaitone SA, Qushawy M, and Elsherbiny NM
- Subjects
- Animals, Aorta pathology, Caspase 3 metabolism, Chalcones isolation & purification, Diabetes Mellitus, Experimental complications, Diabetic Angiopathies drug therapy, Diabetic Angiopathies pathology, Disease Progression, Glycyrrhiza chemistry, Inflammation pathology, Male, NF-E2-Related Factor 2 metabolism, Oxidative Stress drug effects, Rats, Signal Transduction drug effects, Streptozocin, Aorta drug effects, Chalcones pharmacology, Diabetes Mellitus, Experimental drug therapy, Inflammation drug therapy
- Abstract
Objectives: The current study provides evidence on the ameliorative impact of Isoliquiritigenin (ISL), a natural bioflavonoid isolated from licorice roots against diabetes mellitus (DM)-induced aortic injury in rats., Methods: DM was induced in male Sprague-Dawley rats by single I.P. injection of STZ (50 mg/kg). ISL was administrated daily (20 mg/kg, orally) for 8 wks., Key Findings: Diabetic group showed a significant aortic injury with evidence of atherosclerotic lesions development. Daily ISL (20 mg/kg, orally) administration for 8 wks significantly restored aortic oxidative/antioxidative stress homeostasis via modulating NrF-2/Keap-1/HO-1. Moreover, ISL treatment restored aortic levels of IL-10 and dampened aortic levels of IL-6 and TNF-α. Caspase-3 expression significantly declined as well. Further, ISL treatment successfully suppressed aortic endothelin-1 (ET-1) expression and restored NO contents, eNOS immunostaining paralleled with retraction in atherosclerotic lesions development, and lipid deposition with histopathological architectural preservation and restoration of almost normal aortic thickness., Conclusion: ISL can be proposed to be an effective protective therapy to prevent progression of DM-induced vascular injury and to preserve aortic integrity., (© The Author(s) 2021. Published by Oxford University Press on behalf of the Royal Pharmaceutical Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
- Published
- 2021
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