冠心病合并心力衰竭患者血浆组织蛋白酶S和血小板反应蛋白-1的表达及意义
摘要
目的探讨冠心病合并心力衰竭患者血浆组织蛋白酶S(Cat S)和血小板反应蛋白-1(TSP-1)的表达与该病的关系及意义。方法选取2017年3月至2018年4月期间本院老年病科收治确诊的120例冠心病(CHD)患者为研究组,并根据是否合并心力衰竭(HF)分为CHD+HF组和无合并HF的CHD组,纳入同时期30例健康体检者为对照组。采用酶联免疫法(ELISA)检测各组血浆中Cat S、TSP-1浓度,使用彩色多普勒超声仪检测被试者的心功能指标;利用Pearson相关性分析Cat S、TSP-1与心功能指标的关系,采用非条件logistic多元回归分析冠心病合并心力衰竭的危险因素。结果研究组的FS、EF、ESV和CK-MB明显低于对照组(P <0. 05),EDV、Cat S、TSP-1和NT-proBNP、hs-CRP明显高于对照组(P <0. 05); CHD+HF组各心功能分级患者血浆Cat S、TSP-1水平明显高于单纯CHD组(P <0. 05),且Ⅳ级患者血浆Cat S、TSP-1水平明显高于Ⅱ级和Ⅲ级(P <0. 05),Ⅲ级明显高于Ⅱ级(P <0. 05);相关性分析表明,冠心病合并心力衰竭患者血浆Cat S与TSP-1水平呈正相关(P <0. 01),血浆Cat S和TSP-1水平与FS、EF、ESV、CK-MB均呈负相关(P <0. 05),与EDV、NT-proBNP、肌钙蛋白I(c Tn I)呈正相关(P <0. 05);回归分析结果显示,ESV、Cat S和TSP-1、NT-proBNP、c Tn I、CK-MB是冠心病合并心力衰竭发生的危险因素(OR=3. 048,3. 354,3. 014,2. 153,3. 231,2. 344,P均<0. 05)。结论冠心病合并心力衰竭患者血浆Cat S和TSP-1的表达水平明显升高,其可能参与调控冠心病合并心力衰竭的发生发展过程,推测二者可为临床冠心病合并心力衰竭的预测及诊治提供一定的参考价值。
引文
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[3]蔡丹磊,黄荫浩,刘东华,等.参麦注射液和阿托伐他汀治疗冠心病慢性心力衰竭的疗效分析[J].辽宁中医杂志,2016,43(12):2587-2589.
[4] Reddy AT,Lakshmi SP,Muchumarri RR,et al. Nitrated Fatty Acids Reverse Cigarette Smoke-Induced Alveolar Macrophage Activation and Inhibit Protease Activity via Electrophilic S-Alkylation[J]. PLo S One,2016,11(4):e0153336. DOI:10. 1371/journal. pone. 0153336.
[5] Kong P,Cavalera M,Frangogiannis NG. The role of thrombospondin(TSP)-1 in obesity and diabetes[J]. Adipocyte,2014,3(1):81-84. DOI:10. 4161/adip. 26990.
[6]中华医学会心血管病学分会,中华心血管病杂志编辑委员会.中国心力衰竭诊断和治疗指南2014[J].中华心血管病杂志,2014,42(2):98-122. DOI:10. 3760/cma. j. issn. 0253-3758.2014. 02. 004.
[7] Apostolakis E,Akinosoglou K. Reexamining the New York Heart association functional classification of heart failure[J]. Am J Cardiol,2007,100(5):911-912. DOI:10. 1016/j. amjcard. 2007.05. 006.
[8]颜红兵.临床冠心病诊断与治疗指南[M].北京:人民卫生出版社,2010:8-26.
[9]秦练,李桂花,王忠,等.冠心病合并心力衰竭患者血清HO-1/CO系统水平变化及其意义[J].重庆医学,2017,46(10):1343-1345. DOI:10. 3969/j. issn. 1671-8348. 2017. 10. 014.
[10]宋鹏飞,陶向荣.老年慢性心力衰竭患者血脂水平与心功能关系临床观察[J].中国老年保健医学,2014,12(3):60-61.DOI:10. 3969/j. issn. 1672-4860. 2014. 03. 026.
[11] Pawar K,Sharbati J,Einspanier R,et al. Mycobacterium bovis BCG Interferes with miR-3619-5p Control of Cathepsin S in the Process of Autophagy[J]. Front Cell Infect Microbiol,2016,6:27. DOI:10. 3389/fcimb. 2016. 00027.
[12]高磊,何国平,钱亿超,等.急性冠脉综合征患者血小板反应蛋白-1基因多态性分析[J].中国循证心血管医学杂志,2016,8(12):1449-1451. DOI:10. 3969/j. issn. 1674-4055. 2016. 12.10.
[13] Li X,Cheng XW,Hu L,et al. Cathepsin S activity controls ischemia-induced neovascularization in mice[J]. Int J Cardiol,2015,183:198-208. DOI:10. 1016/j. ijcard. 2015. 01. 058.
[14] Figueiredo JL,Aikawa M,Zheng C,et al. Selective cathepsin S inhibition attenuates atherosclerosis in apolipoprotein E-deficient mice with chronic renal disease[J]. Am J Pathol,2015,185(4):1156-1166. DOI:10. 1016/j. ajpath. 2014. 11. 026.
[15] Oresic BK,Ofori L,van der Linden WA,et al. Design of a highly selective quenched activity-based probe and its application in dual color imaging studies of cathepsin S activity localization[J]. J Am Chem Soc,2015,137(14):4771-4777. DOI:10. 1021/jacs.5b00315.
[16] Wilkinson RD,Young A,Burden RE,et al. A bioavailable cathepsin S nitrile inhibitor abrogates tumor development[J]. Mol Cancer,2016,15:29. DOI:10. 1186/s12943-016-0513-7.
[17] Anderson DR,Dunbar M,Murnaghan J,et al. Aspirin or Rivaroxaban for VTE Prophylaxis after Hip or Knee Arthroplasty[J]. N Engl J Med,2018,378(8):699-707. DOI:10. 1056/NEJMoa1712746.
[18] Dong XQ,Yu WH,Zhu Q,et al. Changes in plasma thrombospondin-1 concentrations following acute intracerebral hemorrhage[J]. Clin Chim Acta,2015,450:349-355. DOI:10. 1016/j. cca. 2015. 09. 013.
[19]张永兴.血小板反应蛋白1/2及其类似物调节血管化的分子基础和临床应用进展[J].医学综述,2016,22(9):1669-1673.DOI:10. 3969/j. issn. 1006-2084. 2016. 09. 002.