STEMI血清可溶性ST2、CTRP9表达水平及其相关性研究
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摘要
目的测定急性ST段抬高型心肌梗死(STEMI)患者血清中可溶性生长刺激表达因子(s ST2)、C1q/肿瘤坏死因子相关蛋白9(CTRP9)表达水平变化,分析两者的相关性。方法选取佳木斯大学附属第一医院心血管内科2016年11月到2017年8月期间住院患者90名,其中STEMI患者44名为实验组(STEMI组),稳定型心绞痛患者46名为对照组;入选患者均记录一般临床资料、心肌损伤标志物、血脂及肌酐等相关生化指标;采用ELISA测定血清s ST2、CTRP9水平;进行统计学分析。结果 STEMI组血清中s ST2水平显著高于对照组,P<0.01,STEMI组血清中CTRP9水平显著低于对照组,P<0.05。STEMI组血清中s ST2与CTRP9呈负相关(r=-0.462,P<0.05)。结论急性ST段抬高型心肌梗死患者血清s ST2明显升高,CTRP9明显降低,两者之间具有负相关性。
Objective The levels of soluble growth stimulating factor( s ST2) and C1 q/tumor necrosis factor-related protein 9( CTRP9) in serum of patients with acute ST-segment elevation myocardial infarction( STEMI) were measured and their correlations were analyzed. Methods Ninety patients hospitalized in the department of cardiology of first affiliated hospital of Jiamusi University from November 2016 to August 2017 were enrolled in this study,44 of them were selected as STEMI group( experimental group) and 46 were selected as stable STEMI group( control group). General clinical data,myocardial injury markers,serum creatinine and other biochemical indicators of all selected patients were recorded. Serum s ST2 and CTRP9 levels were measured by ELISA. All data collected were statistical analyzed.Results The level of s ST2 in serum of STEMI group was significantly higher than that of control group( P<0.01),and the level of CTRP9 in serum of STEMI group was significantly lower than that of control group( P<0.05). The concentration of s ST2 was negatively correlated with CTRP9 in STEMI group( r =-0.462,P<0.05).Conclusions Serum s ST2 was significantly increased in patients with acute ST-elevation myocardial infarction, CTRP9 was significantly decreased. There was a negative correlation between them.
Objective The levels of soluble growth stimulating factor( s ST2) and C1 q/tumor necrosis factor-related protein 9( CTRP9) in serum of patients with acute ST-segment elevation myocardial infarction( STEMI) were measured and their correlations were analyzed. Methods Ninety patients hospitalized in the department of cardiology of first affiliated hospital of Jiamusi University from November 2016 to August 2017 were enrolled in this study,44 of them were selected as STEMI group( experimental group) and 46 were selected as stable STEMI group( control group). General clinical data,myocardial injury markers,serum creatinine and other biochemical indicators of all selected patients were recorded. Serum s ST2 and CTRP9 levels were measured by ELISA. All data collected were statistical analyzed.Results The level of s ST2 in serum of STEMI group was significantly higher than that of control group( P<0.01),and the level of CTRP9 in serum of STEMI group was significantly lower than that of control group( P<0.05). The concentration of s ST2 was negatively correlated with CTRP9 in STEMI group( r =-0.462,P<0.05).Conclusions Serum s ST2 was significantly increased in patients with acute ST-elevation myocardial infarction, CTRP9 was significantly decreased. There was a negative correlation between them.
引文
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[2]Lax A,Sanchez-Mas J,Asensio-Lopez MC,et al.Mineralocorticoid receptor antagonists modulate galectin-3 and Interleukin-33/ST2 signaling in left ventricular systolic dysfunction after acute myocardial Infarction[J].JACC Heart Fail,2015,3(1):50-58.
[3]Tu X,Nie SF,Liao YH,et al.The IL-33-ST2L Pathway is associated with coronary artery disease in a Chinese Hanpopulation[J].Am J Hum Gen,2013,93:652-660.
[4]王霞,张秀明.可溶性ST2在心力衰竭中的临床应用前景[J].国际检验医学杂志,2015,36(3):387-389.
[5]Kambara T,Ohashi K,Shibata R,et al.CTRP9 protects against myocardial injury following ischemia-reperfusion through AMPKdependent mechanism.J Biol Chem.2012,287:18965-18973.
[6]Uemura Y,Shibata R,Ohashi K,et al.Adipose-derived factor CTRP9 attenuates vascular smooth muscle cell pro-liferation and neointimal formation[J].FASEB J,2013,27(1):25-33.
[7]Sun Y,Yi W,Yuan Y,et al.C1q/tumor necrosis fac-tor-related protein-9,a novel adipocyte-derived cyto-kine,attenuates adverse remodeling in the ischemicmouse heart via protein kinase A activation[J].Circulation,2013,128(26):113-120.