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Objective:To explore the relationships between the endothelial microparticles (EMPs)in peripheral blood and CD4+ CD25 + Foxp3+ regulatory T cells and their cytokine levels in the patients with acute coronary syndrome (ACS),and to clarify the mechanism of EMPs in the pathogenesis of ACS by affecting the Treg cell differentiation and function.Methods:Twenty-three patients with stable angina (SAP)were allocated to SAP group,and 52 patients with ACS were allocated to ACS group.Twenty individuals with normal conventional coronary angiography results were recruited as control group.The levels of EMPs and the percents of CD4+ CD25 +Foxp3+ regulatory T cells in peripheral blood of the patients in various groups were measured by flow cytometry. The expressions of Foxp3 mRNA and the plasma levels of TGF-β1 were detected with Real-Time PCR and ELISA, respectively.Correlation analysis was performed between EMPs and regulatory T cells,Foxp3 mRNA expression level and TGF-β1 level.Results:Compared with control group and SAP group,the level of EMPs in peripheral blood of the patients in ACS group was increased significantly,but the percentage of regulatory T cells,the Foxp3 mRNA expression level and the plasma TGF-β1 level were decreased markedly (P <0.01).The correlation analysis showed that there were significantly negative correlation between EMPs and regulatory T cells,Foxp3 mRNA expression level and TGF-β1 level (r = - 0.452,P = 0.001;r = - 0.466,P = 0.001;r = - 0.555,P = 0.000 ). Conclusion:EMPs may involve in the process of occurrence and development of ACS and plaque instability by regulating the differentiation and function of CD4+ CD25 + Foxp3 + regulatory T cells.
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Objective To study influence of tongxinluo on blood endothelial microparticles(EM Ps) and matrix metalloprotei‐nase‐9(MMP‐9) in patients with acute myocardial infarction after percutaneous coronary intervention(PCI) .Methods One hundred and twenty‐eight hospitalized patients with acute myocardial infarction after per‐cutaneous coronary intervention were recruited from January 2012 to December 2014 ,All patients were randomly divided into tongxinluo group (n=65) and control group (con‐ventional treatment ,n=63) .Tongxinluo group was on the basis of conventional treatment group with tongxinluo capsules 2 plus ,3 times a day .We detected the EMPs and MMP‐9 of two groups preoperatively and on the 7th postoperatively day .Results Com‐pared with the conventional treatment group ,blood EMPs and MMP‐9 in tongxinluo group were lower after 7 days treatment ,the difference was statistically significant (P<0 .05) .There was a positive correlation between the EMPs and MMP‐9(P<0 .05) .Con‐clusion For patients with acute myocardial infarction after percu‐taneous coronary intervention ,tongxinluo could further inhibit in‐flammatory reaction ,make the plaque stability and improve the function of endothelial cells on the basis of conventional treatment groups .
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BACKGROUND:Occluder implantation in patients with congenital heart disease can increase in vivo platelet adhesion and aggregation, resulting in thrombosis on the occluder surface. OBJECTIVE:To investigate the effect of the occluder on platelet function in patients with congenital heart disease undergoing transcatheter closure. METHODS: Clinical data from 124 patients with congenital heart disease undergoing transcatheter closure were retrospectively analyzed. These patients were divided into groups of atrial septal defect in 46 cases, patent ductus arteriosus in 43 cases and ventricular septal defect in 35 cases according to the types of congenital heart disease. The positive rates for peripheral blood CD62p, CD63 RESULTS AND CONCLUSION:There was no difference in the positive rates of peripheral blood CD and thrombin sensitive protein were compared before and 6 hours, 24 hours, 12 months after occluder implantation. 62p, CD63 and thrombin sensitive protein among three groups prior to occluder implantation. Up to 6 hours after occluder implantation, the expression levels of peripheral blood CD62p, CD63 and thrombin sensitive protein reached peak in the three groups, especialy in the patients with atrial septal defect and ventricular septal defect, then gradualy decreased. After 12 months, the expression levels of CD62p and CD63 recovered in the patients with patent ductus arteriosus and ventricular septal defect, but stil maintained a higher level in those with atrial septal defect (P < 0.05). The expression of thrombin sensitive protein showed no difference among the three groups at different time. These findings indicate that after occluder implantation, the platelet activation is more remarkable and lasts longer in the patients with atrial septal defect and ventricular septal defect, especialy in those with ventricular septal defect.
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Objective To investigate the effects of aggressive dosing of atorvastatin on the expression of SOCS1 in CD4 + Tlymphocytes from patients with unstable angina pectoris during peri-operative period of PCI.Methods A cohort of 50 patients with unstable angina pectoris were randomized (random number) to give pretreatment with either an aggressive dose (80 mg/d,n =25) or a routine dose (20 mg/d,n =25)of atorvastatin.Circulating CD4 +T cells were subsequently obtained prior to PCI,and also 18 h to 24 hours after PCI,using a magnetic cell sorting system (MACS).Fluorescence-based quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure expressions of SOCSI mRNA in the isolated CD4 + Tlymphocytes,and western blot analysis was used to detect levels of SOCS1 protein.Serum levels of IFN-γwere quantified using enzyme-linked immunosorbent assays (ELISAs).Results Compared with routine dose group,the expressions of SOCS1 mRNA and protein levels were dramatically increased and those were higher in aggressive dose group following PCI (P ＜ 0.05).In contrast,serum levels of IFN-γsignificantly increased following PCI in both groups,but it was higher in routine dose group than in aggressive dose group (P ＜ 0.05).Conclusions Treatment with aggressive dosing of atorvastatin reduced the post-PCI myocardial inflammatory response in patients with unstable angina pectoris,possibly modulating by up-regulating SOCS1 expression in CD4 + Tlymphocytes.
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Objective To investigate the effects of large dose of atorvastatin on the expression of Sprouty-1 in CD4 + T lymphocytes from unstable angina patients during perioperative period of PCI.Methods A total of 52 unstable angina patients enrolled were divided randomly (random number) into large-dose atorvastatin (80 mg/d,n =26) pretreated group and moderate-dose atorvastatin (20 mg/d,n =26) pretreated group.Circulating CD4 + T cells were obtained by magnetic cell sorting system (MACS) before PCI and 18-24h after PCI.For detecting the gene expression,the reverse transcription fluorescent quantitative polymerase chain reaction (RT-PCR) was used to measure the expression of Sprouty-1 mRNA in CD4 + T lymphocyte.The level of Sprouty-1 protein was detected with Western blot analysis and IL-2 was quantified by enzyme-linked immunosorbent assay (ELISA).Results ①Compared with large-dose group before PCI,the expression of Sprouty-1 mRNA and Sprouty-1 protein levels were dramatically increased in large-dose group after PCI (P ＜ 0.05).②Compared with moderate-dose group before PCI,the expression of Sprouty-1 mRNA and protein levels were slightly increased in moderate-dose group after PCI,but there was no statistical significance (P ＞ 0.05).③Compared with large-dose group before PCI,the serum level of IL-2 was decreased in large-dose group after PCI (P ＜ 0.05).Whereas the serum level of IL-2 was slightly increased in moderate-dose group after PCI compared to moderate-dose group before PCI,there was still no statistical significance (P ＞ 0.05).Conclusions Large-dose atorvastatin pretreatment reduced post-PCI myocardial inflammation through up-regulating the expression of Sprouty-1 mRNA and level of Sprouty-1 protein in CD4 + T lymphocytes.
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ObjectiveTo inyestigate the effect of miRNA-155 expression on the differentiations and functions of CD4 + T lymphocyte in patients with unstable angina pectoris. MethodsTwenty-one patients with unstable angina pectoris (UAP) were enrolled in this study, and another 18 patients with normal coronary arteries evidenced by angiography were assigned as control group. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression of miRNA-155 in CD4 + T lymphocyte of the peripheral blood. And the levels of IFN-γ and IL-4 in serum were determined by using enzyme-linked immunosorbent assay (ELISA). The CD4 + T lymphocyte were isolated from mononuclear cells prepared with Ficoll-Hypaque density-gradients centrifugation from human peripheral blood by magnetic cell sorting system. Then, the CD4 +T cells (2 × 106 cells/mL) were seeded in culture plates with 6 wells.The CD4 + T lymphocytes were divided into 3 groups in experiment: control group, miRNA-155 group, and miRNA-155 inhibitor group. The numbers of Th1 and Th2 cells were measured by flow cytometry analysis (FACS).The protein levels and expressions of IFN-γRα, T-bet, GATA-3 mRNA were measured by using western blotting and qRT-PCR, respectively. The levels of IFN-γ and IL-4 in culture supernatants of CD4 +T lymphocytes were detected by using ELISA. ResultsIn comparison with the control group, there was significant increase in the expression of miRNA-155 and serum level of IFN-γ in the UAP group (P ＜0. 01 ). There was a positive correlation between miRNA-155 and serum IFN-γ ( r =0. 842, P ＜ 0. 0l ).However, in vitro, the number of Th1, the protein level and expression of T-bet mRNA, and supernatant IFN-γ increased, and the protein level and expression of IFN-γRα protein decreased in miRNA-155 group in comparison with the control group (all P ＜0. 01 ). Interestingly, there were no significant differences in the number of Th2 cells, the expressions of GATA-3mRNA and IFN-γRα mRNA, GATA-3 protein and supernatant IL-4 between control group and miRNA-155 group ( all P ＞ 0. 05 ). And the miRNA-155 inhibitor could attenuate the effect of miRNA-155 effectively. ConclusionsThe miRNA-155 can promote differentiations and improve the function of Thl, playing an important role in the pathogenesis of unstable angina pectoris.
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Objective To investigate the dynamic changes of cardiomyocyte apoptosis and Caspase-12 activation after coronary microembolization (CME) in rats. Methods The CME models were produced by injection of 42 μm microspheres (3000/0.1 ml) into the left ventricle during clampinduced ascending aorta occlusion for 10 seconds in adult male Sprague-Dawley rats (CME group).The sham-operation group was injected with saline instead (S group). The survivors were randomly divided into five groups: 3 h, 6 h, 12 h, 24 h and 4 weeks (n=10, each), respectively. In addition,10 rats were designed as normal control group. Cardiomyocyte apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. The expressions of Caspase-3, 12 and procaspase-3 and 12 were detected with Western-blot analysis. The activity of Caspase-12 was determined with fluorometric assay kit. Results (1)Compared with the shamoperation group and normal control group, the apoptosis rates of cardiomyocytes in CME group were significantly increased at each time point respectively (all P＜0.05). Apoptotic cardiomyocytes were found mainly in the border zones and infarct foci. The apoptosis rates of cardiomyocytes at 3 h, 6 h,12 h, 24 h and 4 weeks after CME were (1.76±0.68)%, (3.17±1.26)%, (1.34±0.12)%,(1.07±0.65)% and (0.30±0.13)%, respectively. The apoptosis rates of cardiomyocytes increased at 3 h after CME, peaked at 6 h after CME (all P＜0.05), and then gradually decreased with lowest value at 4 weeks (all P＜0.01). (2)Compared with sham-operation group and normal control group,the relative activation level of Caspase-3 and 12 in CME group increased remarkably (all P＜0.05).The time courses of Caspase-3 and 12 expressions corresponded well to those of cardiomyocyte apoptosis after CME. Conclusions The amount of cardiomyocytes apoptosis is significantly increased after CME. Caspase-12 may be involved in the apoptosis of cardiomyocyte after CME.