The Influence of Vitamin A Supplementation on Foxp3 and TGF-β Gene Expression in Atherosclerotic Patients

The aim of this study was to investigate the role of vitamin A in Foxp3 and TGF-β gene expression in atherosclerotic patients. Patients and healthy controls in the vitamin A group received 25,000 IU retinyl palmitate per day, while patients in the placebo group took one capsule of placebo per day fo...

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Veröffentlicht in:Journal of nutrigenetics and nutrigenomics 2012-01, Vol.5 (6), p.314-326
Hauptverfasser: Mottaghi, Azadeh, Salehi, Eisa, Keshvarz, Ali, Sezavar, Hashem, Saboor-Yaraghi, Ali-Akbar
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Sprache:eng
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Zusammenfassung:The aim of this study was to investigate the role of vitamin A in Foxp3 and TGF-β gene expression in atherosclerotic patients. Patients and healthy controls in the vitamin A group received 25,000 IU retinyl palmitate per day, while patients in the placebo group took one capsule of placebo per day for 4 months. Gene expressions of regulatory T cells were studied by real-time PCR. The levels of Foxp3 expression in phytohemagglutinin-activated cells were much higher in the patients who received vitamin A than in placebo-treated patients and healthy controls, while Foxp3 gene expression in oxidized low-density lipoprotein-activated cells showed no significant differences between all groups (p = 0.357). A significant difference in the expression level of TGF-β gene in fresh cells was observed between patients and healthy controls (p = 0.009). TGF-β gene expression in oxidized low-density lipoprotein-activated cells increased in all groups; however, these changes were not statistically significant (p = 0.65); the changes obtained were 2.8-, 2.2- and 3.9-fold in the vitamin A, placebo, and control groups, respectively. Based on suppressing actions of regulatory T cells on effector T cells and findings that show that vitamin A has the effect of increasing expression of regulatory T cells, it can be concluded that supplementation with vitamin A in atherosclerotic patients may be effective in slowing disease progression.
ISSN:2504-3161
2504-3188
1661-6758
DOI:10.1159/000341916