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目的探讨强化剂量阿托伐他汀治疗对急性冠状动脉综合征(acute coronary syndrome,ACS)行经皮冠状动脉介入术(percutaneous coronary intervention,PCI)治疗患者外周血内皮细胞微粒(endothelial microparticles,EMP)水平和CD4~+CD25~+Foxp3~+调节性T细胞及细胞因子水平的影响。方法行PCI治疗的ACS患者104例,根据治疗方法分为阿托伐他汀强化治疗组(强化组)和阿托伐他汀常规治疗组(常规组)各52例。常规组PCI术前、术后均口服阿托伐他汀20mg/d,强化组PCI术前口服阿托伐他汀80mg/d,术后40mg/d。分别于术前、术后1周检测2组外周血EMPs水平、CD4~+CD25~+Foxp3~+调节性T细胞百分率、Foxp3mRNA和转化生长因子-β1(transforming growth factor-β1,TGF-β1)表达水平,分析EMPs与CD4~+CD25~+Foxp3~+调节性T细胞百分率、Foxp3mRNA和TGF-β1水平的相关性。结果强化组和常规组术后CD4~+CD25~+Foxp3~+调节性T细胞百分率[(4.62±0.51)%、(3.85±0.60)%]、Foxp3 mRNA[(224.2±10.9)%、(173.7±11.6)%]和TGF-β1[(305.2±33.9)、(214.6±36.1)ng/L]均高于术前[(3.19±0.55)%、(3.25±0.49)%,(99.9±8.2)%、(101.2±9.4)%,(159.8±32.8)ng/L、(167.3±38.2)ng/L],EMPs水平[(1 062.2±336.8)个/μL、(1 387.8±353.6)个/μL]低于术前[(1 661.9±346.5)个/μL、(1 647.4±368.2)个/μL](P<0.01),且强化组较常规组变化更明显,差异有统计学意义(P<0.01);EMPs与CD4~+CD25~+Foxp3~+调节性T细胞百分率、Foxp3mRNA和TGF-β1水平均呈负相关(r=-0.526,P=-0.000;r=-0.487,P=-0.001;r=-0.581,P=0.000)。结论强化剂量阿托伐他汀治疗可能通过下调EMPs水平,从而上调CD4~+CD25~+Foxp3~+调节性T细胞和TGF-β1水平,进而减轻炎症反应,稳定斑块。
Objective To investigate the effects of intensive-dose atorvastatin on peripheral blood mononuclear cells (EMPs) in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) CD4 ~ + CD25 ~ + Foxp3 ~ + regulatory T cells and cytokines levels. Methods A total of 104 ACS patients undergoing PCI were divided into two groups according to the therapy: 52 patients in the atorvastatin intensive treatment group and the atorvastatin conventional treatment group. Conventional group before and after oral administration of atorvastatin 20mg / d, intensive group before PCI oral atorvastatin 80mg / d, postoperative 40mg / d. The level of EMPs, percentage of CD4 ~ + CD25 ~ + Foxp3 ~ + regulatory T cells, Foxp3mRNA, and transforming growth factor-β1 (TGF-β1) The levels of EMPs and the percentage of CD4 ~ + CD25 ~ + Foxp3 ~ + regulatory T cells, Foxp3mRNA and TGF-β1 were analyzed. Results The percentages of CD4 ~ + CD25 ~ + Foxp3 ~ + regulatory T cells in the intensive and conventional groups were significantly higher than those in the control group [(4.62 ± 0.51)%, (3.85 ± 0.60)%], Foxp3 mRNA [(224.2 ± 10.9)%, (3.19 ± 0.55)%, (3.25 ± 0.49)% and (99.9 ± 8.2)%, respectively, compared with those in the control group (± 11.6% and TGF-β1 [305.2 ± 33.9 and 214.6 ± 36.1] ng / (101.2 ± 9.4)%, (159.8 ± 32.8) ng / L and (167.3 ± 38.2) ng / L, respectively) and the levels of EMPs [(1 062.2 ± 336.8) / μL, (1 387.8 ± 353.6) ] Was lower than that of preoperative [(6661.9 ± 346.5) / μL, (16447.4 ± 368.2) /μL] (P <0.01), and the changes in the intensive group were more obvious than those in the conventional group (P < 0.01). The percentage of EMPs and CD4 ~ + CD25 ~ + Foxp3 ~ + regulatory T cells, Foxp3mRNA and TGF-β1 were negatively correlated (r = -0.526, P = -0.000; r = -0.487, P = -0.001 ; r = -0.581, P = 0.000). Conclusions Forty doses of atorvastatin may reduce the level of EMPs and upregulate the levels of CD4 ~ + CD25 ~ + Foxp3 ~ + regulatory T cells and TGF-β1, thereby reducing the inflammatory reaction and stabilizing the plaque.