Abstract
Oxidative stress is a common condition described in risk factors for cardiovascular disease. Betanin, a bioactive pigment from red beetroot demonstrates anti-inflammatory and antioxidant properties. The main aim of this study was to evaluate the short-term intake of betanin against oxidative stress in a rodent model, a common condition described in several risk factors for cardiovascular disease. Oxidative stress was induced in Wistar rats by a hyperlipidemic diet for 60 days, followed by betanin administration (20 mg·kg−1) through oral gavage for 20 days. Plasma biochemical parameters and antioxidant enzyme activities were evaluated. Lipid peroxidation and histopathological changes were determined in the liver. The hyperlipidemic diet caused hyperglycemia, hyperinsulinemia, insulin resistance, and increases in alanine transaminase and aspartate transaminase levels. Oxidative stress status was confirmed by reduction of antioxidant enzyme activities, increased lipid peroxidation, and liver damage. Purified betanin regulated glucose levels, insulin, and insulin resistance. Hepatic damage was reversed as evidenced by the reduction in alanine transaminase and aspartate transaminase levels and confirmed by histological analyses. Betanin reduced hepatic malondialdehyde and increased superoxide dismutase, catalase, and glutathione peroxidase activities. Short-term betanin intake modulated biochemical parameters, reversed hepatic tissue damage, and attenuated oxidative stress in Wistar rats.
Highlights
Cardiovascular diseases (CVD) are the worldwide leading cause of death
HOMA-IR, total cholesterol (TC), TG, and aspartate transaminase (AST) increased after phase 1 in the animal group fed the HF60 when compared to the group fed the CONT 60 (Table 2)
The high-fat diet offered for 60 days led to changes in glucose metabolism, an increase in insulin resistance confirmed by HOMA-IR, increased cholesterol and triglyceride plasma levels, and liver damage confirmed by histopathological analyses
Summary
Cardiovascular diseases (CVD) are the worldwide leading cause of death They comprise a class of disorders that involve blocking blood supply to cardiac muscle and the brain due to the presence of inflammatory cells, such as macrophages and T lymphocytes, as well as deposition of oxidized lipids in the vascular wall of blood vessels [1,2]. Disorders such as coronary heart and cerebrovascular diseases are the major clinical manifestations of CVD [3]. ROS are constantly generated in the mitochondrial respiratory chain and play an important role as regulatory mediators in signaling processes, cell proliferation and defense, and gene expression, their excess, caused by an imbalance
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