Effects of resveratrol in the activity of matrix metalloproteinase (MMP)-2 via reduction of oxidative stress in a model of vascular remodelling associated to metabolic syndrome in rats

• Grant number: 23/16327-0
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): June 01, 2024
• Effective date (End): December 31, 2024
• Field of knowledge: Biological Sciences - Pharmacology - Cardiorenal Pharmacology
• Principal Investigator: Michele Mazzaron de Castro
• Grantee: Leandro Bianchoni Manoel
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

Obesity is a global public health problem and is associated with the secretion of pro-inflammatory adipokines that contribute to metabolic syndrome and associated cardiovascular diseases, such as hypertension. Visfatin is one of these adipokines and can cause oxidative stress in the vasculature. It is already known that oxidative stress contributes to arterial remodeling through different pathways, such as increasing the activity and expression of NF-kB, the main transcription factor for MMP-2. MMP-2 (extracellular matrix metalloproteinase) plays a role in hypertension, being essential in the maladaptive remodeling. Arterial stiffness precedes the onset of cardiovascular diseases in animals and individuals with obesity associated with metabolic syndrome. Therefore, the increase in visfatin may be associated with arterial remodeling by increasing MMP-2 activity via NF-kB activation and oxidative stress. The use of antioxidants is increasingly being studied in experimental and clinical models aiming to improve vascular dysfunctions caused by high blood pressure. Thus, taking into account the antioxidant capacity of resveratrol and its protective effects on the cardiovascular system, the hypothesis of the present study is that the use of resveratrol improves vascular remodeling and dysfunction that precedes hypertension in a model of obesity and metabolic syndrome in rats, by decreasing oxidative stress, visfatin and MMP-2 activity.