Background: Obesity is a polyetiological condition characterized by excessive adiposity, resulting from a disequilibrium between energy intake and energy expenditure. High-fat diets (HFDs) have been identified as key drivers of the obesity epidemic and its comorbidities. Butin, a natural flavonoid with antioxidant and oxidative stress-modulating properties, has been proposed as a potential therapeutic agent for obesity. This study investigated the efficacy of butin against HFD-induced obesity in rats.

Methods: Thirty Wistar rats were orally administered butin diluted with 0.5% sodium carboxymethyl cellulose for 30 days. The rats were randomly divided into five groups: typical diet, HFD control, HFD + 10 mg/kg butin, HFD + 20 mg/kg butin, and 20 mg/kg butin alone. At the end of the study, biochemical parameters including lipid profile [total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL)], liver function test [alanine aminotransferase (ALT), aspartate aminotransferase (AST)], kidney test [creatinine, blood urea nitrogen (BUN)], free fatty acid (FFA), as well as antioxidant activity [superoxide dismutase (SOD), glutathione (GSH), catalase (CAT), and malonaldehyde (MDA)], were performed. Furthermore, pro-inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6)], concentrations of serum insulin, leptin, ghrelin, adiponectin (ADP), and fibroblast growth factor 15 (FGF15) were also evaluated.

Results: Butin exhibited substantial efficacy in mitigating HFD-induced obesity in rats. Butin administration resulted in a statistically significant reduction in the levels of TG, TC, TNF-α, IL-1β, IL-6, MDA, ALT, AST, BUN, and creatinine, while simultaneously elevating the levels of HDL, SOD, GSH, and CAT. Moreover, butin significantly modulated serum insulin, leptin, ghrelin, ADP, FFA, and FGF15 suggesting its potential for managing obesity-related metabolic and inflammatory markers. Analysis of the data revealed that butin treatment could regulate potential biomarkers and other metabolic pathways associated with HFD-induced obesity in rats.

Conclusion: Butin may attenuate hyperlipidemia and protect against HFD-induced obesity in rats through a pleiotropic mechanism of action. Additionally, butin may serve as an alternative clinical supplement to ameliorate obesity complications.

Background: Oxidative stress is a potential cause of cardiovascular pathologies, so the protection of endothelial cells and vascular tissues is essential to avoid such conditions, perhaps with the use of natural compounds rich in phenolic compounds with a proven high antioxidant capacity. The present study was designed to show the cytoprotective capacity of phenolic extracts from the plant Brunfelsia grandiflora, as well as describe its antioxidant defense mechanisms and the expression of some molecular markers involved in cellular protection.

Methods: Human EA.hy926 cells were exposed to Brunfelsia grandiflora (B. grandiflora) extract (1, 10, 25, 50, 100, and 200 μg/mL) in co-treatment (22 h with 100 μM tert-Butyl hydroperoxide (t-BOOH) and B. grandiflora concentrations) and pre-treatment (18 h of B. grandiflora concentrations and then 200 μM t-BOOH for 4 h). Cell viability, reactive oxygen species (ROS) production, nitric oxide (NO) levels, caspase 3/7 activity, malondialdehyde (MDA) concentration, and reduction in reduced glutathione (GSH) levels, glutathione peroxidase (GPx), and glutathione reductase (GR) activity were measured, and real-time PCR molecular assays superoxide dismutase (SOD2), nuclear factor E2-related factor (NRF2), BCL-2-associated X protein (BAX), and B-cell lymphoma 2 (BCL2) were performed. Data were analyzed via one-way ANOVA followed by Tukey's post hoc test.

Results: B. grandiflora bark extract, mainly at concentrations of 25, 50, 100, and 200 μg/mL, significantly (p < 0.05) reversed (pre-treatment and co-treatment) the deleterious effects of t-BOOH on EA.hy926 endothelial cells, which were significantly decreased cell viability, GSH activity, and SOD2 and NRF2 expression (p < 0.05); and significantly increased levels of ROS, NO, MDA, caspase-3/7 activity, GPx activity, GR activity, and the BAX/BCL2 ratio (p < 0.05).

Conclusions: B. grandiflora extract was able to reduce the deleterious effects of t-BOOH on EA.hy926 endothelial cells, which may indicate its potential phytotherapeutic benefit against cytotoxic damage caused by chemical agents.