Vegetable-derived fatty acids may protect against arterial thrombosis
MedWire News: Dietary intake of the omega-3 (n-3) fatty acid (FA) α-linolenic acid (ALA) - found at high concentrations in vegetable oils - impairs arterial thrombus formation, tissue factor (TF) expression, and platelet activation in mice, Swiss research shows.
These findings suggest that plant-derived ALA may represent "an attractive cardioprotective alternative" to fish-derived n-3 FAs, which may be hard to access in many countries due to limited availability or unfavorable geographic conditions, remark Felix Tanner (University of Zurich) and colleagues.
"Experimental and epidemiological studies have extensively characterized the cardioprotective and antithrombotic effects of the fish-derived dietary long-chain omega-n-3 FAs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)," the researchers explain.
Following oral intake, ALA is partially converted into EPA and DHA, but its effect on arterial thrombus formation is unknown.
To investigate, Tanner and team fed male C57Bl/6 mice a diet containing either 7.3% ALA (high-ALA diet) or 0.03% ALA (low-ALA diet) for 2 weeks.
At the end of the 2 weeks, ALA levels in the aorta of animals fed the high-ALA diet were markedly higher than those in the low-ALA group, at 14.9% versus 0.14% of total FA content. In contrast, EPA and DHA levels did not differ between the two groups, suggesting that any antithrombotic effects would be a direct result of ALA activity, say the researchers.
The team found that, after photochemical injury, arterial thrombus formation was significantly delayed in mice fed a high-ALA diet compared with those on a low-ALA diet, with a mean occlusion time of 68 versus 40 minutes.
Furthermore, thrombin-induced platelet aggregation was inhibited in mice fed a high-ALA diet, with maximal aggregation and area under the curve significantly lower, and lag time significantly higher in the high-ALA group compared with the low-ALA group. Similar results were observed for collagen-induced aggregation.
Mice in the high-ALA group also had had significantly lower arterial TF expression, TF activity, nuclear factor-κB activity and p38 mitogen-activated protein kinase activation in platelets than mice in the high-ALA group. These findings suggest that direct inhibition of TF in via p38 and NF-κB seems to play a major role in ALA's effect on arterial thrombus formation, write Tanner and co-authors in the journal Arteriosclerosis, Thrombosis, and Vascular Biology.
They conclude that the study "provides solid evidence for a potent dual antithrombotic effect of an ALA-rich diet by reducing platelet activation and impairing vascular TF expression."
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By Laura Dean