Effects of Baru Almond Oil (Dipteryx alata Vog.) Treatment on Thrombotic Processes, Platelet Aggregation, and Vascular Function in Aorta Arteries.

Background: This study assessed the effects of Baru (Dipteryx alata Vog.) almond oil supplementation on vascular function, platelet aggregation, and thrombus formation in aorta arteries of Wistar rats. Methods: Male Wistar rats were allocated into three groups. The control group (n = 6), a Baru group receiving Baru almond oil at 7.2 mL/kg/day (BG 7.2 mL/kg, n = 6), and (iii) a Baru group receiving Baru almond oil at 14.4 mL/kg/day (BG 14.4 mL/kg, n = 6). Baru oil was administered for ten days. Platelet aggregation, thrombus formation, vascular function, and reactive oxygen species production were evaluated at the end of treatment. Results: Baru oil supplementation reduced platelet aggregation (p < 0.05) and the production of the superoxide anion radical in platelets (p < 0.05). Additionally, Baru oil supplementation exerted an antithrombotic effect (p < 0.05) and improved the vascular function of aorta arteries (p < 0.05). Conclusion: The findings showed that Baru oil reduced platelet aggregation, reactive oxygen species production, and improved vascular function, suggesting it to be a functional oil with great potential to act as a novel product for preventing and treating cardiovascular disease.

Yeast carboxymethyl-glucan improves endothelial function and inhibits platelet aggregation in spontaneously hypertensive rats.

Carboxymethyl-glucan is a semi-synthetic derivative of ß-D-glucan, a polysaccharide widely found in several natural sources, such as yeast, fungi, and cereals. This compound has beneficial effects on health and is considered an important immunomodulator. However, studies exploring carboxymethyl-glucan bioactivity in cardiovascular health remain lacking, mainly in hypertension. Thus, this study sought to expand understanding of the effects of carboxymethyl-glucan on vascular and platelet functions in a hypertensive animal model. Spontaneously hypertensive rats and their normotensive Wistar-Kyoto controls were assigned to five groups: control, carboxymethyl-glucan (60 mg kg-1), control spontaneously hypertensive rats, spontaneously hypertensive rats carboxymethyl-glucan (20 mg kg-1), and spontaneously hypertensive rats carboxymethyl-glucan (60 mg kg-1). Animals were treated for four weeks with carboxymethyl-glucan at doses of 20 and 60 mg kg-1 orally, and control rats received saline as a placebo. Vascular reactivity, platelet aggregation, and reactive oxygen species production were evaluated at the end of treatment. The results showed that carboxymethyl-glucan improved vascular function and reduced platelet aggregation, mainly at a 60 mg kg-1 dose. However, despite these effects, there was no reduction in levels of reactive oxygen species. These findings suggested that carboxymethyl-glucan modulates endothelial function. It also acts as a platelet antiaggregant, which is an interesting resource for managing hypertension and its thrombotic complications.

Carboxymethyl-glucan from Saccharomyces cerevisiae reduces blood pressure and improves baroreflex sensitivity in spontaneously hypertensive rats.

Carboxymethyl-glucan (CMG) is a derivative of ß-D-glucan extracted from Sacharomyces cerevisae. This polymer presents improved physicochemical properties and shows health benefits, such as immunomodulation, antioxidant, anti-inflammatory, anti-tumor, and antiplatelet activities, and improved vascular function. However, studies concerning the effect of administration of CMG on the cardiovascular parameters, mainly in the field of hypertension, are scarce. This study aimed to investigate the effect of administration of CMG in spontaneously hypertensive rats (SHR) and normotensive rats (WKY) models. Normotensive and hypertensive animals received CMG at doses of 20 mg kg-1 and 60 mg kg-1 for four weeks. Then, weight gain, lipid profile, renal function, blood pressure, cardiac hypertrophy, baroreflex sensitivity, and sympathetic tone were evaluated. Oral administration of CMG influenced weight gain and cholesterol levels, and significantly reduced urea in the hypertensive animals. It decreased blood pressure levels and cardiac hypertrophy, improved baroreflex response, and reduced the influence of sympathetic tone. The results demonstrate the antihypertensive effect of CMG through improvement in baroreflex sensitivity via sympathetic tone modulation.

N-Salicyloyltryptamine, an N-Benzoyltryptamine Analogue, Induces Vasorelaxation through Activation of the NO/sGC Pathway and Reduction of Calcium Influx.

Benzoyltryptamine analogues act as neuroprotective and spasmolytic agents on smooth muscles. In this study, we investigated the ability of N-salicyloyltryptamine (STP) to produce vasorelaxation and determined its underlying mechanisms of action. Isolated rat mesenteric arteries with and without functional endothelium were studied in an isometric contraction system in the presence or absence of pharmacological inhibitors. Amperometric experiments were used to measure the nitric oxide (NO) levels in CD31+ cells using flow cytometry. GH3 cells were used to measure Ca2+ currents using the whole cell patch clamp technique. STP caused endothelium-dependent and -independent relaxation in mesenteric rings. The endothelial-dependent relaxations in response to STP were markedly reduced by L-NAME (endothelial NO synthase-eNOS-inhibitor), jHydroxocobalamin (NO scavenger, 30 µM) and ODQ (soluble Guanylyl Cyclase-sGC-inhibitor, 10 µM), but were not affected by the inhibition of the formation of vasoactive prostanoids. These results were reinforced by the increased NO levels observed in the amperometric experiments with freshly dispersed CD31+ cells. The endothelium-independent effect appeared to involve the inhibition of voltage-gated Ca2+ channels, due to the inhibition of the concentration-response Ca2+ curves in depolarizing solution, the increased relaxation in rings that were pre-incubated with high extracellular KCl (80 mM), and the inhibition of macroscopic Ca2+ currents. The present findings show that the activation of the NO/sGC/cGMP pathway and the inhibition of gated-voltage Ca2+ channels are the mechanisms underlying the effect of STP on mesenteric arteries.

Modulation of vascular function and anti-aggregation effect induced by (1→3) (1→6)-ß-d-glucan of Saccharomyces cerevisiae and its carboxymethylated derivative in rats.

BACKGROUND: ß-d-Glucans are polysaccharides found in the cell walls of yeasts, such as Saccharomyces cerevisiae, and they have been studied because of their beneficial effects on health, mainly in terms of immunomodulation. However, information on the action of these polymers on vascular and platelet function is still scarce. This study evaluate the effect of (1→3) (1→6) ß-d-glucan (ßG-Sc) and its carboxymethylated derivative (CM-G) on vascular and platelet function in rats. METHODS: The animals received daily oral treatments with ßG-Sc (20mg/kg) and CM-G (20mg/kg) for eight days. Next, cytokine quantification, vascular reactivity and adenosine diphosphate (ADP)- and collagen-induced platelet aggregation studies were performed. In vitro platelet aggregation and P-selectin exposition assays were conducted using 100 and 300µg/mL CM-G. RESULTS: The CM-G-treated group had less IL-8 than did the control. In reactivity experiments, CM-G and ßG-Sc treatments did not change the contractile response of the vessel induced by PHE. Moreover, only CM-G improved the vasorelaxation response to Nitroprusside (SPN, a nitric oxide donor). The in vitro aggregation studies showed that at the highest concentration (300µg/mL), CM-G inhibited the agonist-induced platelet aggregation with an effect similar to that of acetylsalicylic acid and without affecting P-selectin exposition. The treatments with ßG-Sc or CM-G inhibited the platelet aggregation stimulated by ADP, but only ßG-Sc treatment was effective in affect the collagen-stimulated aggregation. CONCLUSIONS: These findings suggest that CM-G modulate positively the vascular function, mainly in responses NO-dependent. CM-G and ßG-Sc have an anti-aggregation effect, being CM-G more selective to ADP-induced platelet aggregation.