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Pine bark extract reduces platelet aggregation
Araghi-Niknam1, Hosseini, Larson
1College of Public Health, University of Arizona, Tucson, AZ, USA
Summary
French maritime pine bark extract (Pycnogenol®) significantly reduced smoke-induced platelet aggregation in smokers over two months. This bioflavonoid supplement lowered platelet reactivity to nonsmoker levels, suggesting a cardiovascular risk reduction.
Area of Science:
- Cardiovascular Pharmacology
- Nutritional Biochemistry
- Hemostasis and Thrombosis
Background:
- Cigarette smoking significantly increases platelet aggregation and reactivity.
- Platelet hyperaggregability is a key risk factor for cardiovascular diseases.
- French maritime pine bark extract (Pycnogenol®) is a bioflavonoid mixture with potential anti-inflammatory and antioxidant properties.
Purpose of the Study:
- To assess the long-term effects of Pycnogenol® on platelet aggregation in cigarette smokers.
- To investigate the impact of Pycnogenol® on smoke-induced changes in platelet function.
- To determine if Pycnogenol® influences thromboxane A2 (TxA2) levels in smokers.
Main Methods:
- A randomized controlled trial involving cigarette smokers and nonsmokers.
- Platelet aggregation was measured before and after smoking, and after 2 months of daily Pycnogenol® supplementation (200 mg/day).
- In vitro platelet aggregation stimulated by platelet-activating factor (PAF) and thromboxane B2 (TxB2) levels were analyzed.
Main Results:
- Two months of daily Pycnogenol® supplementation (200 mg/day) significantly reduced smoke-induced platelet aggregation in smokers to levels observed in nonsmokers.
- Pycnogenol® prevented the smoking-induced increase in thromboxane B2 (TxB2) levels.
- Pycnogenol® did not alter platelet aggregation in nonsmokers or affect in vitro aggregation stimulated by PAF.
Conclusions:
- Long-term consumption of Pycnogenol® effectively reduces platelet aggregation stimulated by tobacco smoke in smokers.
- Pycnogenol® supplementation may mitigate a significant cardiovascular risk factor associated with smoking.
- The mechanism of action appears related to the modulation of thromboxane production rather than direct effects on platelet aggregation pathways.