Li Xiang, Liu Cheng, Cui Jian, Dong Min, Peng Cheng-Hai, Li Qing-Song, Cheng Jia-Li, Jiang Shu-Lin, Tian Ye
Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Basic Clin Pharmacol Toxicol. 2009 Feb;104(2):101-6. doi: 10.1111/j.1742-7843.2008.00340.x. Epub 2008 Dec 16.
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.
本研究旨在调查冠心病患者树突状细胞的功能特征以及普伐他汀对此的影响。48例冠心病患者被分为三组:16例接受每日10mg普伐他汀治疗,16例接受每日20mg普伐他汀治疗,16例未接受普伐他汀治疗。48例冠心病患者(治疗前及治疗4周后)和16名健康个体的树突状细胞取自外周血。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培养基中的细胞因子水平。测量血脂和高敏C反应蛋白。与正常组相比,冠心病患者中表达CD86+的树突状细胞更多,且冠心病患者树突状细胞的免疫刺激能力更强。混合淋巴细胞反应中冠心病患者的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反应蛋白显著相关,但与低密度脂蛋白胆固醇无关。两种剂量的普伐他汀均显著抑制树突状细胞的功能并降低C反应蛋白,这与降低血浆胆固醇无关。普伐他汀的抗炎作用在两个剂量组之间无明显差异。总之,冠心病中树突状细胞被激活,树突状细胞介导的免疫机制可能参与冠心病的发病机制。普伐他汀可抑制树突状细胞激活,这与降低血浆胆固醇无关。不同剂量的普伐他汀在抑制树突状细胞功能方面无明显差异。