{'fraction_non_alphanumeric': 0.02454873646209386, 'fraction_numerical': 0.020938628158844765, 'mean_word_length': 5.132743362831858, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Vitamin E potentiates the antiplatelet activity of aspirin in collagen-stimulated platelets.

BACKGROUND AND OBJECTIVES
The combination of vitamin E with aspirin is becoming an attractive therapeutic approach to prevent thrombotic vascular accidents. In this study we investigated the capacity of vitamin E (50 and 100 M) to enhance the antiplatelet effect of aspirin.


DESIGN AND METHODS
The dose-response curves of platelet aggregation, dense body secretion, phospholipase C activation and calcium mobilization were measured in aspirin-treated platelets with and without added vitamin E (50 and 100 M). The role of vitamin E in reducing platelet adhesion to collagen was also studied.


RESULTS
We demonstrated that, in platelets incubated with 100 M vitamin E, collagen-concentration ( g/mL) able to induce 50% of the maximal platelet aggregation and of the calcium mobilization was higher than in controls (11.6 versus 3.8 and 21.3 versus 9.8, respectively). Furthermore, 50 M vitamin E reduced platelet adhesion to collagen by about 80%.


INTERPRETATION AND CONCLUSIONS
These data demonstrate that vitamin E can potentiate the antiplatelet activity of aspirin by inhibiting the early events of platelet activation pathways induced by collagen. This finding provides a rationale for combining aspirin and vitamin E to prevent thrombotic complications in atherosclerotic patients.