Alternative therapies in health and medicine · 2020
Assessment of in vitro Effects of Anthocyanins on Platelet Function.
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Gaiz Almottesembellah, Kundur Avinash R, Colson Natalie, Shibeeb Sapha, Singh Indu
Аннотация
BACKGROUND: Increased platelet activity plays a significant role in the development of arterial thrombosis and cardiovascular disease (CVD). Natural antioxidants including anthocyanin (AC) have gained considerable interest due to their hypothesized antithrombotic potential.
PRIMARY STUDY OBJECTIVE: Our study aimed to examine the in vitro effect of AC compounds on platelet activation and aggregation.
METHODS: Fasting blood samples were collected from healthy volunteers (n = 13). A full blood examination was done to exclude any abnormal specimen. Flow cytometer assessed platelet activity by recording platelet surface markers expression of P-selectin (CD62P) and PAC-1. Platelet aggregation studies were performed by stimulating platelets using three different agonists adenosine diphosphate (ADP), collagen and arachidonic acid (AA).
SETTING: The study was done in the school of Medical Sciences, Griffith University.
PARTICIPANTS: Thirteen healthy adult participants were involved for blood collection.
INTERVENTION: AC was prepared using hemicellulose capsules sourced from Bilberries and Black Currants.
RESULTS: Anthocyanin (50 mg/L) significantly inhibited AA-induced platelet aggregation. Expression of P-selectin was significantly suppressed by 50 mg/L AC as measured by flow cytometer.
CONCLUSIONS: AC attenuates platelet function by suppressing P-selectin expression and influencing Thromboxane A2 pathway (AA stimulation). These results provide further evidence for the effect of AC and the possible mechanism by which AC reduces platelet aggregation and activation. This study supports future human intervention trials to show that AC may act as a complement to other antiplatelet agents in reducing the risk of thrombosis.
PRIMARY STUDY OBJECTIVE: Our study aimed to examine the in vitro effect of AC compounds on platelet activation and aggregation.
METHODS: Fasting blood samples were collected from healthy volunteers (n = 13). A full blood examination was done to exclude any abnormal specimen. Flow cytometer assessed platelet activity by recording platelet surface markers expression of P-selectin (CD62P) and PAC-1. Platelet aggregation studies were performed by stimulating platelets using three different agonists adenosine diphosphate (ADP), collagen and arachidonic acid (AA).
SETTING: The study was done in the school of Medical Sciences, Griffith University.
PARTICIPANTS: Thirteen healthy adult participants were involved for blood collection.
INTERVENTION: AC was prepared using hemicellulose capsules sourced from Bilberries and Black Currants.
RESULTS: Anthocyanin (50 mg/L) significantly inhibited AA-induced platelet aggregation. Expression of P-selectin was significantly suppressed by 50 mg/L AC as measured by flow cytometer.
CONCLUSIONS: AC attenuates platelet function by suppressing P-selectin expression and influencing Thromboxane A2 pathway (AA stimulation). These results provide further evidence for the effect of AC and the possible mechanism by which AC reduces platelet aggregation and activation. This study supports future human intervention trials to show that AC may act as a complement to other antiplatelet agents in reducing the risk of thrombosis.