Ellagic Acid prevents vascular dysfunction in small mesenteric arteries of ovariectomized hypertensive rats

• Published in: The Journal of nutritional biochemistry 2022-07, Vol.105, p.108995-108995, Article 108995
• Main Authors: da Silva, Fabrício Bragança, Romero, Walckiria Garcia, Rouver, Wender do Nascimento, Silva, Katiane, de Almeida, Simone Alves, Mengal, Vinícius, Peluso, Antonio Augusto, Endlich, Patrick Wander, Bissoli, Nazaré Souza, Claudio, Erick Roberto Gonçalves, de Abreu, Gláucia Rodrigues
• Format: Article
• Language: English
• Subjects: Animals; Cardiovascular Diseases - metabolism; Catalase - metabolism; Elagic acid; Ellagic Acid - metabolism; Ellagic Acid - pharmacology; endothelium dysfunction; Endothelium, Vascular - metabolism; Estradiol - pharmacology; Female; Humans; Hypertension - metabolism; menopause; Mesenteric Arteries; Nitric Oxide - metabolism; Nitric Oxide Synthase Type III - metabolism; oxidative stress; Rats; Rats, Inbred SHR; vascular reactivity; Vasodilation
• ISSN: 0955-2863; 1873-4847
• DOI: 10.1016/j.jnutbio.2022.108995

Cardiovascular diseases rank the top causes of death worldwide, with a substantial increase in women compared to men. Such increase can beexplained by the drastic decrease in 17-β-estradiol hormone during menopause and associated with endothelium-dependent vascular dysfunction. The current treatments for cardiovascular diseases (e.g., hypertension), are only palliative and therefore, feasible, non-invasive options for preventing further vascular damage are needed. The polyphenol ellagic acid (EA) has risen as a candidate with possible vascular protection properties. This study evaluated the effects of EA in small mesenteric arteries of ovariectomized spontaneously hypertensive rats. Our findings showed that EA oral treatment for 4 weeks preserved vasodilation endothelial-dependent in acetylcholine pre-constricted arteries of spontaneously hypertensive rats to the same extent as 17-β-estradiol treatment, an effect that was abolished in the presence of the nitric oxide synthase inhibitor L-NitroG-L-Arginine Methyl Ester. Moreover, EA induced vascular nitric oxide release, by increasing both the activitation site phosphorylation and total levels of the endothelial nitric oxide synthase. Finally, EA decreased superoxide anion while increased total levels of the antioxidant enzymes Superoxide Dismutase 2 and catalase. We concluded that EA has vasodilation properties acting via endothelial nitric oxide synthase activation and a potential antioxidant effect by stimulating the Superoxide Dismutase 2-catalase pathway. [Display omitted]