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Effects of pravastatin on the function of dendritic cells in patients with coronary heart disease.

机译:普伐他汀对冠心病患者树突细胞功能的影响。

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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.
机译:这项研究的目的是研究冠心病患者树突状细胞的功能概况以及普伐他汀对此的影响。 48例冠心病患者分为三组:16例普伐他汀10毫克/天治疗,16例普伐他汀20毫克/天治疗和16例不使用普伐他汀治疗。来自48名冠心病患者(治疗前和治疗后4周)和16名健康个体的树突状细胞来自外周血。通过流式细胞术评估树突状细胞的CD86。通过混合淋巴细胞反应测量树突状细胞的免疫刺激能力。分析混合淋巴细胞反应介质中的细胞因子水平。测量血脂和高敏C反应蛋白。与正常组相比,冠心病中CD86 +树突状细胞表达更多,并且树突状细胞在冠心病中具有更高的免疫刺激能力。混合性淋巴细胞反应中冠心病的T淋巴细胞分泌较高水平的促炎细胞因子和较低水平的抗炎细胞因子。 CD86表达与C反应蛋白显着相关,但与低密度脂蛋白胆固醇不相关。两种剂量的普伐他汀均可显着抑制树突状细胞的功能并降低C反应蛋白,这与血浆胆固醇的降低无关。普伐他汀的抗炎作用在两个剂量组之间没有明显差异。总之,树突状细胞在冠心病中被激活,树突状细胞介导的免疫机制可能与冠心病的发病机制有关。普伐他汀可以抑制树突状细胞的活化,这与血浆胆固醇的降低无关。普伐他汀在不同剂量下对树突状细胞功能的抑制作用无明显差异。

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