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急性冠状动脉综合征患者炎性因子的变化及苯那普利的干预作用
引用本文:谢萍,曹云山,苏鹏,李玉红,张世魁,Mathias M.Borst. 急性冠状动脉综合征患者炎性因子的变化及苯那普利的干预作用[J]. 中华老年心脑血管病杂志, 2012, 14(11): 1152-1154
作者姓名:谢萍  曹云山  苏鹏  李玉红  张世魁  Mathias M.Borst
作者单位:1. 甘肃省人民医院心血管病研究中心,兰州,730000
2. 德国海德堡大学Caritas医院心脏科
基金项目:兰州市科技局重点支持项目
摘    要:目的探讨急性冠状动脉综合征(ACS)患者血清炎性因子变化及苯那普利稳定动脉粥样硬化斑块的可能机制。方法入选70例ACS患者为ACS组,并随机分为苯那普利治疗组40例和常规治疗组30例;同时又分稳定性心绞痛(SAP)组22例,对照组32例。比较各组Toll样受体4(TLR4)、TNF-α、基质金属蛋白酶9(MMP-9)表达差异及其相关性。结果 ACS组TLR4、TNF-α和MMP-9含量显著高于SAP组和对照组(P<0.01)。治疗4周后,苯那普利治疗组TLR4、TNF-α和MMP-9含量明显低于常规治疗组(P<0.05)。结论血管紧张素转换酶抑制剂苯那普利可能通过抑制ACS患者TLR4过度表达及其下游炎性细胞因子TNF-α和MMP-9分泌,稳定ACS易损斑块,改善其预后。

关 键 词:急性冠状动脉综合征  Toll样受体4  肿瘤坏死因子α  基质金属蛋白质酶9  心绞痛  血管紧张素Ⅱ

Change of inflammation factors in patients with acute coronary syndrome and its intervention with benazepril
Affiliation:XIE Ping,CAO Yun-shan,SU Peng,et al (Research Center of Cardiovascular Disease,Gansu Provincial People’s Hospital,Lanzhou 730000,Gansu Province,China)
Abstract:Objective To study the change of serum inflammatory factors in patients with acute coronary syndrome(ACS) and the possible mechanism of benazepril in stablizing atherosclerostic plaques.Methods Seventy ACS patients were randomly divided into benazepril treatment group (n= 40) and routine treatment group(n = 30).in addition,22 patients with stable angina pectoris (SAP) served as a SAP group and 32 subjects served as control group.Expressions of TLR4, TNF-αand MMP-9 in different groups and their correlation were compared.Results The expression levels of TLR4,TNF-αand MMP-9 were significantly higher in ACS group than in SAP group and control group and significantly lower in benazepril treatment group than in routine treatment group(P<0.05,P<0.01).Conclusion Benazepril can stabilize the valnerable atherosclerostic plaques in ACS patients and improve their prognosis by down-regulating the over-expression of TLR4 and reducing the TNF-αand MMP-9 secretion in its down stream.
Keywords:acute coronary syndrome  Toll-like receptor 4  tumor necrosis factor-alpha  matrix metalloproteinase 9  angina pectoris  angiotensin Ⅱ
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