Alamandine attenuates oxidative stress in the right carotid following transverse aortic constriction in mice

• Published in: Peptides (New York, N.Y. : 1980) Vol. 171; p. 171094
• Main Authors: de Lima Sanches, Bruno, Souza-Neto, Fernando, de Alcântara-Leonídeo, Thaís Cristina, Silva, Mário Morais, Guatimosim, Silvia, Vieira, Maria Aparecida Ribeiro, Santos, Robson Augusto Souza, da Silva, Rafaela Fernandes
• Format: Journal Article
• Language: English
• Published: United States 01.01.2024
• Subjects: Animals; Carotid Arteries - surgery; Constriction; Disease Models, Animal; Male; Mice; Mice, Inbred C57BL; Oxidative Stress; Ventricular Remodeling; Alamandine; Oxidative stress; Transverse aortic constriction; Vascular remodelling; Renin-angiotensin system
• ISSN: 0196-9781; 1873-5169
• DOI: 10.1016/j.peptides.2023.171094

Pressure overload can result in significant changes to the structure of blood vessels, a process known as vascular remodeling. High levels of tension can cause vascular inflammation, fibrosis, and structural alterations to the vascular wall. Prior research from our team has demonstrated that the oral administration of alamandine can promote vasculoprotective effects in mice aorta that have undergone transverse aortic constriction (TAC). Furthermore, changes in local hemodynamics can affect the right and left carotid arteries differently after TAC. Thus, in this study, we aimed to assess the effects of alamandine treatment on right carotid remodeling and the expression of oxidative stress-related substances induced by TAC. Male C57BL/6 mice were categorized into three groups: Sham, TAC, and TAC treated with alamandine (TAC+ALA). Alamandine treatment was administered orally by gavage (30 µg/kg/day), starting three days before the surgery, and continuing for a period of fourteen days. Morphometric analysis of hematoxylin and eosin-stained sections revealed that TAC induced hypertrophic and positive remodeling in the right carotid artery. Picrosirius Red staining also demonstrated an increase in total collagen deposition in the right carotid artery due to TAC-induced vascular changes. Alamandine treatment effectively prevented the increase in reactive oxygen species production and depletion of nitric oxide levels, which were induced by TAC. Finally, alamandine treatment was also shown to prevent the increased expression of nuclear factor erythroid 2-related factor 2 and 3-nitrotyrosine that were induced by TAC. Our results suggest that alamandine can effectively attenuate pathophysiological stress in the right carotid artery of animals subjected to TAC.