Why the study?
Does exposure to docosahexaenoic acid and eicosapentaenoic acid reduce platelet-mediated thrombin generation and thrombus formation in human platelets and mouse models?
Does exposure to docosahexaenoic acid and eicosapentaenoic acid reduce platelet-mediated thrombin generation and thrombus formation in human platelets and mouse models?
Docosahexaenoic acid and eicosapentaenoic acid reduce platelet-mediated thrombin generation and attenuate thrombus formation in preclinical models, supporting their cardioprotective value.
n-3 PUFAs may attenuate platelet thrombin generation and thrombus formation; leaves open clinical antithrombotic translation.
Omega-3 polyunsaturated fatty acids (n-3 PUFAs) are associated with a variety of cellular alterations that mitigate cardiovascular disease. However, pinpointing the positive therapeutic effects is challenging due to inconsistent clinical trial results and overly simplistic in vitro studies. Here we aimed to develop realistic models of n-3 PUFA effects on platelet function so that preclinical results can better align with and predict clinical outcomes. Human platelets incubated with the n-3 PUFAs docosahexaenoic acid and eicosapentaenoic acid were stimulated with agonist combinations mirroring distinct regions of a growing thrombus. Platelet responses were then monitored in a number of ex-vivo functional assays. Furthermore, intravital microscopy was used to monitor arterial thrombosis and fibrin deposition in mice fed an n-3 PUFA-enriched diet. We found that n-3 PUFA treatment had minimal effects on many basic ex-vivo measures of platelet function using agonist combinations. However, n-3 PUFA treatment delayed platelet-derived thrombin generation in both humans and mice. This impaired thrombin production paralleled a reduced platelet accumulation within thrombi formed in either small arterioles or larger arteries of mice fed an n-3 PUFA-enriched diet, without impacting P-selectin exposure. Despite an apparent lack of robust effects in many ex-vivo assays of platelet function, increased exposure to n-3 PUFAs reduces platelet-mediated thrombin generation and attenuates elements of thrombus formation. These data support the cardioprotective value of-3 PUFAs and strongly suggest that they modify elements of platelet function in vivo.
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Adili et al. (2017) studied this question.
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