(PTFS15-03-24) Characterization of Polyphenols in Baru (Dipteryx alata) and Their Effects on Palmitic Acid-Induced Oxidative Stress in Rat Aortic Vascular Smooth Muscle Cells

Objectives: Hyperlipidemia is a major modifiable risk factor for cardiovascular disease. As cholesterol accumulates along the vascular wall, atherosclerotic plaques form, which can decrease blood flow. Oxidative stress, an imbalance between reactive oxygen species (ROS) and antioxidants, can exacerbate inflammation and trigger apoptosis in vascular smooth muscle cells (VSMCs), contributing to atherogenesis. Baru nuts, a type of legume native to Brazil, are rich in bioactive compounds such as polyphenols, and its consumption has been shown to improve lipid profile in mildly hypercholesterolemic subjects. However, the mechanisms through which baru nuts exert their health benefits remain elusive. Thus, we aimed to assess the effects of baru nut polyphenols on palmitic acid-induced oxidative stress in aortic VSMCs.

Methods: Polyphenols were extracted from ground, roasted baru nuts using 80% ethanol in an ultrasonic bath followed by identification and quantification using liquid chromatography with tandem mass spectrometric detection (LC-MS/MS). Male rat aortic VSMCs were incubated with 400 µg/mL baru nut polyphenol extract (BPE) for 1 h prior to a 24-h treatment with 100 µM palmitic acid (PA). Expression of prooxidant, xanthine oxidase (XO), and antioxidant, heme oxygenase (HO)-1, enzymes were assessed via western blot. Protein expression was quantified then analyzed with one-way ANOVA followed by Tukey post-hoc multiple comparisons analysis. Significance was set at P ≤ 0.05.

Results: Ellagic acid and gallic acid were found to be the most abundant polyphenols in BPE (3732.54 ± 1904.06 and 131.39 ± 53.67 µg/g of ground roasted baru nut, respectively). Small amounts of protocatechuic acid and cyanidin 3-rutinoside were also present. Expression of XO was increased in the cells treated with PA alone (P = 0.003) compared to control but decreased with BPE relative to the PA group, albeit not significantly. This suggests BPE is protecting against PA-mediated increases in XO expression and ROS. HO-1 expression was increased in the BPE group (P = 0.002).

Conclusions: Our findings suggest that BPE may help to protect against PA-induced oxidative stress in VSMCs. Further experiments aiming to explore the effects of BPE on PA-induced inflammation and apoptosis in VSMCs are underway.

Funding Sources: We thank the NIH MARC program.