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SUMO特异性蛋白酶1在心肌组织缺血/再灌注损伤中的保护作用 被引量:1

Protective Effect of SUMO-Specific Protease 1 on Ischemia/Reperfusion Injury of Myocardial Tissue
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摘要 目的探讨SUMO特异性蛋白酶1(SENP1)在心肌组织缺血/再灌注损伤中的保护作用。方法选取14例行体外循环心脏手术前、后的右心房组织,建立缺血再灌注小鼠模型,通过实时定量PCR检测患者和大鼠心肌组织SENP1的mRNA变化。对H9C2细胞株进行缺氧复氧处理后检测LDH释放率,观察细胞死亡情况。结果实时定量PCR结果显示,14例患者缺血再灌注后心肌组织内SENP1 mRNA含量为(4.845±1.248),较灌注前明显升高(P<0.01)。单纯缺血处理的小鼠心肌SENP1 mRNA含量较正常组小鼠略高,且随着灌注时间的延长,SENP1 mRNA含量呈逐渐递增的趋势。特异性siRNA敲除大鼠心肌细胞H9C2细胞内SENP1 48 h后SENP1mRNA水平降至对照组的30%以下,敲除SENP1的H9C2细胞在缺氧及复氧处理后LDH释放增加。结论SENP1在心肌缺血再灌注中有保护作用,缺乏SENP1可能会加重心肌损伤。 Objective To investigate the protective effect of SUMO-specific protease 1( SUMO-SENP1) on ischemia / reperfusion injury of myocardial tissue. Methods Fourteen cases of right atrial tissue before and after cardiopulmonary bypass heart operation were selected,the mouse model of ischemia reperfusion was established,and real-time quantitative polymerase chain reaction( PCR) was used to detect the changes of SENP1 mRNA in myocardial tissue of patients and rats. The LDH release rate was detected after hypoxia reoxygenation on H9C2 cell line,and the cell death was observed. Results The results of real-time PCR showed that the SENP1 mRNA content in myocardial tissue of 14 cases after reperfusion was( 4. 845 ± 1. 248),which was significantly higher than that before reperfusion( P〈0. 01). The SENP1 mRNA content in myocardium of ischemia treatment rats was slightly higher than that of normal rats,and increased with the increasing reperfusion time. The mRNA level of SENP1 in H9C2 cells of specific siRNA knockout rats decreased to 30% of the controls 48 hours later,and LDH release in H9C2 cells of knockout SENP1 increased after hypoxia reoxygenation. Conclusion SENP1 has protective effects on myocardial ischemia reperfusion. The lack of SENP1 might aggravate the myocardial injury.
作者 顾剑民 薛松
出处 《广西医学》 CAS 2014年第11期1526-1528,1537,共4页 Guangxi Medical Journal
关键词 心肌缺血 SUMO特异性蛋白酶1 心肌缺血再灌注损伤 低氧诱导因子 Myocardial ischemia SUMO-specific protease 1 Ischemia/reperfusion injury Hypoxia-inducible factor
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