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Effects of Pravastatin on the Function of Dendritic Cells in Patients with Coronary Heart Disease
Author(s) -
Li Xiang,
Liu Cheng,
Cui Jian,
Dong Min,
Peng ChengHai,
Li QingSong,
Cheng JiaLi,
Jiang ShuLin,
Tian Ye
Publication year - 2009
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2008.00340.x
Subject(s) - pravastatin , cd86 , dendritic cell , medicine , mixed lymphocyte reaction , inflammation , immune system , immunology , lymphocyte , t cell , cholesterol
The aim of the study was to investigate the functional profile of dendritic cells in patients with coronary heart disease and the effects of pravastatin on this. Forty‐eight patients with coronary heart disease were divided into three groups: 16 treated with pravastatin 10 mg/day, 16 treated with pravastatin 20 mg/day and 16 not treated with pravastatin. Dendritic cells from 48 patients with coronary heart disease (before and 4 weeks after the treatment) and 16 healthy individuals were derived from peripheral blood. CD86 of dendritic cells was assessed by flow cytometry. Immunostimulatory capacity of dendritic cells was measured by mixed lymphocyte reaction. The levels of cytokines in the medium of mixed lymphocyte reaction were analysed. Blood lipids and high‐sensitivity C‐reactive protein were measured. Compared to normal group, more CD86+ dendritic cells were expressed in coronary heart disease and greater immunostimulatory capacity of dendritic cells in coronary heart disease was demonstrated. T lymphocytes in coronary heart disease in mixed lymphocyte reaction secreted higher levels of pro‐inflammation cytokines and lower levels of anti‐inflammation cytokines. CD86 expression significantly correlated with C‐reactive protein, but did not correlate with low‐density lipoprotein cholesterol. Both dosages of pravastatin markedly inhibited the function of dendritic cells and lowered C‐reactive protein, which is independent of plasma cholesterol lowering. The anti‐inflammatory effect of pravastatin showed no obvious difference between the two dosage groups. In conclusion, dendritic cells were activated in coronary heart disease and dendritic cell‐mediated immune mechanisms may be involved in the pathogenesis of coronary heart disease. Pravastatin can inhibit dendritic cell activation, which is independent of plasma cholesterol lowering. Pravastatin in different doses showed no apparent differences in the inhibition of dendritic cell functions.