增强型体外反搏对稳定性劳累型心绞痛外周血单个核细胞损伤的影响  

Effect of Enhanced External Counterpulsation on PBMC Injury in Patients with Stable Angina Pectoris

作　　者：谢天鸽 谢天飞 刘云[1] 段继豪[1] XIE Tian-ge;XIE Tian-fei;LIU Yun;DUAN Ji-hao(Department of Cardiology,Luohe Third People’s Hospital,Luohe 462300,China;Department of Medicine,Henan Medical College,Xinzheng 451191,China)

机构地区：[1]漯河市第三人民医院心内科,河南漯河462300 [2]河南医学高等专科学校医学系,河南新郑451191

出　　处：《河南科技大学学报（医学版）》2019年第3期192-195,208,共5页Journal of Henan University of Science & Technology:Medical Science

摘　　要：目的探讨增强型体外反搏(EECP)对稳定性劳累型心绞痛患者外周血单个核细胞(PBMC)的活性和炎症的影响。方法选择2015年1月至2018年1月在河南省漯河市第三人民医院心内科接受治疗的484例稳定性劳累型心绞痛患者,依据随机数字表法分为两组,对照组241例接受6周常规治疗;观察组243例接受6周体外反搏联合常规治疗。观察两组临床疗效,分析血清及脂多糖刺激PBMC后上清液中的IL-6、Hs-CRP、IL-1β水平,比较PBMC以及脂多糖刺激PBMC后TLR4、MyD88和NF-κBp6mRNA的表达水平。结果观察组临床总有效率优于对照组,差异有统计学意义(P<0.05),心绞痛缓解、运动耐量增加以及心绞痛缓解且运动耐量增加的比例明显高于对照组(P<0.05)。观察组血清及脂多糖刺激PBMC后上清液中的IL-6、Hs-CRP、IL-1β水平低于对照组;未接受脂多糖刺激的PBMCTLR4、MyD88和NF-κBp65mRNA的表达水平低于对照组,差异有统计学意义(P<0.05);接受脂多糖刺激后,对照组TLR4、MyD88和NF-κBp65mRNA的表达水平变化更加显著。结论EECP可通过调节稳定性劳累型心绞痛患者炎症水平,降低机体损伤,其机制可能与TLR4/NF-κB信号通路有关。Objective To investigate the effect of enhanced external counterpulsation(EECP)on the activity and inflammation of peripheral blood mononuclear cell(PBMC)in patients with stable angina pectoris.Methods From January 2015 to January 2018,484 patients with stable angina pectoris treated in the department of cardiology of the third people’s hospital of Luohe in Henan province were divided into two groups according to the random number table method:241 patients in the control group received routine treatment for 6 weeks and 243 patients in the observation group received external counterpulsation combined with conventional therapy for 6 weeks.Clinical efficacy of the two groups was observed,and the levels of IL-6,Hs-CRP and IL-1βwere detected in serum and the supernatant of PBMC stimulated by lipopolysaccharide,the levels of TLR4,MyD88 and NF-κBp6 mRNA in PBMC and PBMC stimulated by lipopolysaccharide were compared.Results The clinical total effective rate of the observation group was significantly better than that of the control group(P<0.05),and The proportion of angina pectoris relief,increased exercise tolerance,angina pectoris ease and increased exercise tolerance was significantly higher than that of the control group(P<0.05).The levels of IL-6,Hs-CRP and IL-1βin serum and the supernatant of PBMC stimulated by lipopolysaccharide were significantly lower than those in the control group,The expression levels of TLR4,MyD88 and NF-κBp65 mRNA in PBMCs that were not stimulated by lipopolysaccharide were lower than those in the control group(P<0.05).After receiving lipopolysaccharide stimulation,the expression levels of TLR4,MyD88 and NF-κBp65 mRNA in the control group changed more significantly.Conclusion EECP can reduce the body’s injury by regulating the level of inflammation in patients with stable angina pectoris.The mechanism may be related to TLR4/NF-κB signaling pathway.

关 键 词：心绞痛 体外反搏 PBMC 炎症 TLR4/NF-κB信号通路 

分 类 号：R541[医药卫生—心血管疾病]