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Scand J Immunol ; 80(2): 151-7, 2014 Aug.
Article in English | MEDLINE | ID: mdl-24845870

ABSTRACT

Vitamin A is a potential mediator of T helper cells in atherosclerosis. The purpose of this study was to evaluate the effect of vitamin A supplementation on expression of Th17 cells-related IL-17 and RORc genes in atherosclerotic patients. Thirty one atherosclerotic patients and 15 healthy controls were studied for 4 months. Atherosclerotic patients were randomly divided into vitamin A or placebo groups. Healthy controls and patients in vitamin A group received 25,000 IU retinyl palmitate per day. Peripheral blood mononuclear cells were isolated, cultured and divided into three groups including fresh cells, phytohemagglutinin (PHA)-activated T cells and ox-LDL-activated T cells. Gene expressions of T cells were studied by real-time PCR. In atherosclerotic patients, vitamin A supplementation resulted in significant decrease in IL-17 gene expression by 0.63-fold in fresh cell, 0.82-fold in PHA-activated cells and 0.65-fold in ox-LDL-activated cells (P < 0.05 for all). RORc gene expression in fresh cells as well as ox-LDL-activated cells decreased significantly after vitamin A supplementation in atherosclerotic patients (P = 0.0001 for both). In PHA-activated cells, vitamin A supplementation significantly decreased RORc gene in both atherosclerotic patients and healthy subjects by 0.87-fold and 0.72, respectively, while in placebo group, the RORc gene expression significantly increased by 1.17-fold (P < 0.05 for all). Findings of this study suggest that vitamin A supplementation may be an effective approach to slow progression of atherosclerosis.


Subject(s)
Atherosclerosis/drug therapy , Dietary Supplements , Gene Expression/drug effects , Interleukin-17/genetics , Nuclear Receptor Subfamily 1, Group F, Member 3/genetics , Th17 Cells/immunology , Vitamin A/administration & dosage , Atherosclerosis/immunology , Female , Humans , Lipoproteins, LDL , Lymphocyte Activation/immunology , Male , Middle Aged , Phytohemagglutinins , RNA, Messenger/biosynthesis , Th17 Cells/drug effects
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