Fractions from Sea Buckthorn Seeds and Their Bioactive Ingredients as Modulators of Human Blood Platelet Response In Vitro: The Role of Thermal Processing

TL;DR

This study explores how compounds from sea buckthorn seeds, especially after roasting, can reduce platelet activation, potentially helping prevent cardiovascular diseases.

Contribution

The study identifies isorhamnetin derivatives and serotonin as key anti-platelet agents in sea buckthorn seeds, emphasizing the impact of thermal processing.

Findings

Isorhamnetin 3-O-β-glucoside-7-O-α-rhamnoside significantly inhibited platelet activation and prolonged thrombus formation time.

Fractions from roasted sea buckthorn seeds showed greater anti-adhesive effects compared to those from raw seeds.

Serotonin was identified as a major contributor to the anti-platelet activity in roasted seed fractions.

Abstract

Background: Given the pivotal role of diet in cardiovascular diseases (CVDs), there is a growing demand for new sources of bioactive phytochemicals that can contribute to CVD prevention and treatment. Previous research has unveiled the cardioprotective properties of several parts of sea buckthorn (Hippophae rhamnoides L.). For example, various fractions isolated from raw and roasted sea buckthorn seeds showed antioxidant properties in vitro. In addition, the serotonin-rich fraction obtained from roasted seed extract had the strongest antioxidant activity. However, it was unclear which chemical constituents contribute to the anti-platelet potential of sea buckthorn seeds. Methods: The anti-platelet activity of two fractions (fraction b and fraction c) from raw sea buckthorn seed extract, two fractions (fraction d and fraction g) from roasted sea buckthorn seed extract, and two chemical compounds—isorhamnetin 3-O-β-glucoside-7-O-α-rhamnoside (a major component of fraction b), and serotonin (5-HT, 5-hydroxytryptamine), present in fraction c was estimated in several in vitro assays. Results: Isorhamnetin 3-O-β-glucoside-7-O-α-rhamnoside significantly inhibited platelet activation. It lowered the exposition of the active form of GPIIb/IIIa on the surface of 20 μM ADP-stimulated platelets by about 26%. It also inhibited the exposition of P-selectin on the surface of 10 and 20 μM ADP-stimulated platelets. In addition, isorhamnetin 3-O-β-glucoside-7-O-α-rhamnoside (at 50 µg/mL) significantly prolonged the time of thrombus formation. The results also indicate that fractions d and g (from roasted seeds) are more effective anti-adhesive factors than fractions from raw sea buckthorn seeds. Conclusions: It can be suggested that sea buckthorn seeds can serve as a new source of anti-platelet compounds (especially derivatives of isorhamnetin) beneficial in CVD prevention and treatment; however, in vivo research is needed to clarify their mechanism of action, physiologically relevant concentrations, and therapeutic potential.

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