程序性细胞死亡因子4与氨基末端脑利钠肽前体在冠心病猝死者体内的表达及意义
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摘要
目的研究冠心病猝死患者心肌组织中程序性细胞死亡因子4(PDCD4)的表达量与心血中氨基末端脑利钠肽前体(NTproBNP)的表达变化,探讨其在冠心病猝死者体内的表达及意义。方法选取2015年7月~2018年6月于南方医科大学第五附属医院死亡并接受尸检的死亡病例60例,根据尸检结果分为冠心病猝死组(20例)、冠脉狭窄组(20例)以及冠脉正常组(20例),每个病例均收集心肌组织一块用于测定PDCD4的mRNA表达量及蛋白表达量,并抽取右心血样本采用酶联免疫吸附(ELISA)法检测血浆NTproBNP的水平。结果冠心病猝死组心肌组织中PDCD4的mRNA表达量、蛋白表达量均高于另外两组,差异有统计学意义(P<0.05);冠心病猝死组、冠脉狭窄组的血浆NTproBNP含量均高于冠脉正常组,差异有统计学意义(P<0.05);冠心病猝死组的血浆NTproBNP含量高于冠脉狭窄组,差异有统计学意义(P<0.05)。结论 PDCD4、NTproBNP的高表达与冠心病猝死的发生有关,能辅助判定冠心病的严重程度以及协助鉴定冠心病猝死。
Objective To analyse the expression of programmed cell death 4(PDCD4) in myocardial tissues and Amimo-Terminal Pro-Brain Natriuretic Peptide(NTproBNP) in plasma of sudden death patients with coronary heart disease and to discuss its significance. Methods Totally 60 sudden death cases that underwent autopsy in the Fifth Affiliated Hospital of Southern Medical University from July 2015 to June 2018 were collected, and divided into sudden cardiac death with coronary heart disease group(20 cases), single coronary stenosis group(20 cases) and normal control group(20 cases) according to the autopsy results. The myocardial tissue was collected to determine the m RNA expression of PDCD4 as well as the protein expression of PDCD4. NTproBNP in plasma were detected by ELISA. Results The mRNA expression and protein expression of PDCD4 in myocardial tissue of cardiac sudden death with coronary heart disease group were significantly higher than those in the other two groups, the differences were statistically significant(P<0.05). NTproBNP in the sudden cardiac death with coronary heart disease group and single coronary stenosis group was higher than that normal control group, the difference was statistically significant(P<0.05). NTproBNP in the sudden cardiac death with coronary heart disease group was higher than that in the single coronary stenosis group, the difference was statistically significant(P<0.05). Conclusion These indicate that PDCD4 and NTproBNP have a certain guiding role in sudden cardiac death with coronary heart disease. PDCD4 and NTproBNP can help to identify the severity of coronary heart disease and whether it is sudden death due to coronary heart disease.
Objective To analyse the expression of programmed cell death 4(PDCD4) in myocardial tissues and Amimo-Terminal Pro-Brain Natriuretic Peptide(NTproBNP) in plasma of sudden death patients with coronary heart disease and to discuss its significance. Methods Totally 60 sudden death cases that underwent autopsy in the Fifth Affiliated Hospital of Southern Medical University from July 2015 to June 2018 were collected, and divided into sudden cardiac death with coronary heart disease group(20 cases), single coronary stenosis group(20 cases) and normal control group(20 cases) according to the autopsy results. The myocardial tissue was collected to determine the m RNA expression of PDCD4 as well as the protein expression of PDCD4. NTproBNP in plasma were detected by ELISA. Results The mRNA expression and protein expression of PDCD4 in myocardial tissue of cardiac sudden death with coronary heart disease group were significantly higher than those in the other two groups, the differences were statistically significant(P<0.05). NTproBNP in the sudden cardiac death with coronary heart disease group and single coronary stenosis group was higher than that normal control group, the difference was statistically significant(P<0.05). NTproBNP in the sudden cardiac death with coronary heart disease group was higher than that in the single coronary stenosis group, the difference was statistically significant(P<0.05). Conclusion These indicate that PDCD4 and NTproBNP have a certain guiding role in sudden cardiac death with coronary heart disease. PDCD4 and NTproBNP can help to identify the severity of coronary heart disease and whether it is sudden death due to coronary heart disease.
引文
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[21]史洁茹,田成俊,曾强,等.过敏性和冠心病猝死者心肌组织中肥大细胞类胰蛋白酶、脑利钠肽的表达[J].法医学杂志,2016,32(3):161-164.
[22]Vogiatzis I,Dapcevic I,Datsios A,et al.A comparison of prognostic vaule of the levels of pro BNP and troponin Tin patients with acute coronary syndrome(ACS)[J].Med Arch,2016,70(4):269-273.
[23]Struthers AD,George J.High B-type natriuretic peptidehypertensives at target blood pressure:potential role ofβblockers to reduce their elevated risk[J].Hypertension,2015,66(5):927-932.
[2]耿家峰.N端脑钠肽前体、脂蛋白(a)与冠心病患者冠状动脉病变的相关性[J].实用临床医药杂志,2016,20(15):14-16.
[3]Jeong HA,Shin J,Kim E,et al.Correlation of B-type natriuretic peptide levels and echocardiographic parameters in preterm infants with patent ductus arteriosus[J].J Neurol Sci,2016,59(4):183-189.
[4]胡鹏云,杨玉勤.稳心颗粒对冠心病合并心律失常患者QT间期离散度的影响[J].实用心电学杂志,2018,27(2):119-120,124.
[5]刘力,赵文姣.尼沙赫精准心电图与心电图同步分析冠心病改变的临床研究[J].实用心电学杂志,2018,27(1):38-42.
[6]陈伟伟,高润霖,刘力生,等.中国心血管病报告2013概要[J].中国循环杂志,2014,29(7):487-491.
[7]Bajaj A,Rathor P,Sehgal V,et al.Prognostic value of biomarkers in acute non-massive pulmonary embolism:a systematic review and meta-analysis[J].Lung,2015,193(5):639-651.
[8]Lippi G,Sanchis-Gomar F,Cervellin G.Cardiac troponins and mortality in type 1 and 2 myocardial infarction[J].Clin Chem Lab Med,2017,55(2):181-188.
[9]迟晔虹,王雪绒,梁娟,等.老年糖尿病合并冠心病患者的心率变异性分析[J].实用心电学杂志,2017,26(6):420-423.
[10]Ifteni P,Barabas B,Gavris C,et al.Sudden cardiac death:autopsy findings in 7200 cases between 2001 and 2015[J].Am J Forensic Med Pathol,2015,38(1):49-53.
[11]Iribarren C,Chandra M,Rana JS,et al.High-sensitivity cardiac troponin I and incident coronary heart disease among asymptomatic older adults[J].Heart,2016,102(15):1177-1182.
[12]Mc Evoy JW,Chen Y,Ndumele CE,et al.Six-year change in high-sensitivity cardiac troponin T and risk of subsequent coronary heart disease,heart failure,and death[J].JAMA Cardiol,2016,1(5):519-528.
[13]Jaruvongvanich V,Rattanadech W,Damkerngsuntorn W,et al.CK-MB activity,any additional benefit to negative troponin in evaluating patients with suspected acute myocardial infarction in the emergency department[J].J Med Assoc Thai,2015,98(10):935-941.
[14]Sabatasso S,Mangin P,Fracasso T,et al.Early markers for myocardial ischemia and sudden cardiac death[J].Int J Legal Med,2016,130(5):1265-1280.
[15]胡大一,丁荣晶.“胸痛中心”建设中国专家共识[J].中华危重症医学杂志(电子版),2011,4(6):381-393.
[16]Su Q,Li L,Zhou Y,et al.Induction of myocardial PDCD4in coronary microembolization-related cardiac dysfunction:evidence from a large-animal study[J].Cell Physiol Bio chem,2014,34(2):533-542.
[17]Liu X,Cheng Y,Yang J,et al.An essential role of PDCD4in vascular smooth muscle cell apoptosis and proliferation:implications for vascular disease[J].Am J Physiol Cell Physiol,2010,298(6):C1481-C1488.
[18]Ge C,Song J,Chen L,et al.Atheroprotective pulsatile flow induces ubiquitin-proteasome-mediated degradation of programmed cell death 4 in endothelial cells[J].PLoS One,2014,9(3):e91564.
[19]Sheedy FJ,Palsson-McDermott E,Hennessy EJ,et al.Negative regulation of TLR4 via targeting of the proinflammatory tumor suppressor PDCD4 by the micro RNA mi R-21[J].Nat Immunol,2010,11(2):141-147.
[20]Bassan F,Bassan R,Esporcatte R,et al.Very long-term prognostic role of admission BNP in non-ST segment elevation acute coronary syndrome[J].Arq Bras Cardiol,2016,106(3):218-225.
[21]史洁茹,田成俊,曾强,等.过敏性和冠心病猝死者心肌组织中肥大细胞类胰蛋白酶、脑利钠肽的表达[J].法医学杂志,2016,32(3):161-164.
[22]Vogiatzis I,Dapcevic I,Datsios A,et al.A comparison of prognostic vaule of the levels of pro BNP and troponin Tin patients with acute coronary syndrome(ACS)[J].Med Arch,2016,70(4):269-273.
[23]Struthers AD,George J.High B-type natriuretic peptidehypertensives at target blood pressure:potential role ofβblockers to reduce their elevated risk[J].Hypertension,2015,66(5):927-932.