目的 研究mi RNA-223在急性心肌梗死(AMI)患者血清中的表达,并探讨mi R-223表达对心肌细胞凋亡的影响.方法 随机选取2015年1月至2017年1月于新乡市中心医院心血管内科收治的AMI患者67例和同期体检健康人50例,实时荧光定量PCR(RT-q PCR)法检测mi R-223表达水平,以人心肌细胞(HCM)作为模型研究mi R-223表达对HCM凋亡的影响.结果 mi R-223在67例AMI患者血清中的相对表达水平为(5.58±0.99),高于其在50例健康人血清(0.66±0.15)的相对表达水平(P＜0.05),并且经Logistic回归分析显示血清mi R-223是AMI发生的独立危险因素;荧光素酶报告基因系统验证mi R-223靶向抑制HCM细胞中CCTN2基因的表达;经H2O2诱导后,转入mi R-223-mimc的HCM细胞凋亡率比转入mi R-223-NC的HCM细胞凋亡率增加了95.9%.结论 mi R-223在AMI患者血清中高表达,并且高表达的mi R-223可能通过靶向抑制心肌细胞CCTN2的表达而促进其凋亡.
To study the expression of serum micro RNA-223 (mi R-223) and discuss the influence of mi R-223 on cardiac myocyte apoptosis in patients with acute myocardial infarction (AMI). Methods AMI patients (n=67, AMI group) and healthy controls (n=50, control group) were chosen from Department of Cardiovascular Medicine of Xinxiang Central Hospital from Jan. 2015 to Jan. 2017. The expression level of mi R-223 was detected by using real-time fluorescence quantitative polymerase chain reaction (RT-q PCR). The influence of mi R-223 on apoptosis of human cardiac myocytes (HCM) was studied taken HCM as model. Results The expression of mi R-223 was (5.58 ±0.99) in AMI group and (0.66±0.15) in control group (P＜0.05). The results of Logistic regression analysis showed that mi R-223 was an independent risk factor of AMI. Luciferase reporter gene system verified that mi R-223 inhibited the expression of CCTN2 gene in HCM. After H2O2 induction, the apoptosis rate of HCM transfected with mi R-223-mimc increased by 95.9% compared with that of HCM transfected with mi R-223-NC. Conclusion The expression of serum mi R-223 is higher in AMI patients, and high-expressed mi R-223 can improve HCM apoptosis possibly through targeted inhibition of CCTN2 expression in HCM.