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Wiadomosci Lekarskie 2016

Resveratrol more effectively than quercetin reduces endothelium degeneration and level of necrosis factor α in patients with coronary artery disease.

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Natalia I Chekalina
Yuri M Kazakov
Tatyana V Mamontova
Ludmila E Vesnina
Igor P Kaidashev

Mots clés

Abstrait

BACKGROUND

endothelial dysfunction (ED) is one of the most important links in the pathogenesis of atherosclerosis (ASVD) - morphological basis of coronary artery disease (CAD).

OBJECTIVE

to study the effect of polyphenolic antioxidants, resveratrol and quercetin, on endothelial degeneration factors in CAD patients.

METHODS

the study involved 93 patients with coronary artery disease: stable angina pectoris, FC II. The cytofluorometric technique was applied to define the level of circulating endothelial microparticles (EMP) CD32+CD40+ in peripheral blood in order to identify ED. The content of tumor necrosis factor α (TNF-α), fibrinogen, hemocoagulation and lipid profile parameters were being determined in the blood, as well. Patients were divided into 3 groups. Basic therapy (β-blockers, statins, aspirin) was prescribed to 33 persons of the comparison group, patients of the study group 1 (30 persons) additionally received resveratrol at a dose of 100 mg daily, patients of the study group 2 (30 persons) got quercetin at a dose of 3 g per day. In 2 months, the second examination of the patients was performed in the amount indicated.

RESULTS

under the influence of resveratrol a significant reduction of the level of TNF-α and the number of EMP in peripheral blood was shown, in contrast to the results of other study groups. All groups showed a decrease in total cholesterol and low-density lipoprotein cholesterol, statistical differences between data of groups were not found. Indicators of coagulogramma in all study groups did not change significantly, however, there was a statistically significant reduction of fibrinogen in the blood.

CONCLUSIONS

resveratrol, unlike quercetin, has a positive effect on the endothelial function and systemic inflammation, which may be the result of its influence on intracellular molecular cascades associated with the nuclear transcription factor of NF-kB.

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