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过表达Nrf2基因对心肌缺血-再灌注血流动力学和cTnI浓度的影响 被引量:6

The study on the effect from Nrf2 gene overexpression on hemodynamic changes and cardiac troponin I concentration in myocardial ischemia-reperfusion injury model
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摘要 目的探讨过表达核因子(NF)-E2相关因子2(Nrf2)基因对大鼠心肌缺血-再灌注损伤(MIRI)血流动力学和心肌肌钙蛋白I(cTnI)浓度的影响。方法 30只SD大鼠随机分为三组(n=10):假手术组(Sham组)、MIRI组、过表达Nrf2基因组(Nrf2组)。Sham组和MIRI组经冠脉转染携带绿色荧光蛋白的腺病毒载体(Ad-EGFP)至心肌组织,Nrf2组转染携带Nrf2基因的腺病毒载体(Ad-Nrf2)。稳定3d后,三组建立MIRI模型,观察缺血前(T0)、缺血30min(T1)、再灌注30min(T2)和再灌注120min(T3)时HR、左室舒张末期压力(LVEDP)、左室收缩末期压(LVESP)、心室最大压力上升和下降速率(±dp/dtmax)。再灌注120min检测心肌肌钙蛋白I(cTnI)含量。结果与T0时比较,T1~T3时MIRI组、Nrf2组HR明显减慢、LVESP和±dp/dtmax明显降低,LVEDP明显升高(P<0.05)。与Sham组比较,T1~T3时MIRI组、Nrf2组HR明显减慢、LVESP、±dp/dtmax明显降低,LVEDP明显升高(P<0.05)。与MIRI组比较,T1~T3时Nrf2组LVESP和±dp/dtmax明显升高、LVEDP明显降低(P<0.05)。再灌注120min,MIRI组cTnI含量为(6.7±2.5)ng/ml,Nrf2组为(4.6±2.1)ng/ml,明显高于Sham组(1.4±0.4)ng/ml(P<0.05),Nrf2组明显低于MIRI组(P<0.05)。结论大鼠心肌过表达Nrf2基因能够改善心肌缺血-再灌注损伤带来的血流动力学紊乱和抑制cTnI浓度的上升。 Objective To explore the influence {tom the overexpression of nuclear factor E2 related factor2 (Nrfg)gene on the hemodynamie parameters and cardiac troponin I concentration in myocardial ischemia-reperfusion injury(MIRI) model. Methods Thirty SD rats were randomly divided into three groups (n=10): sham operation group(group Sham), myocardial ischemia-reperfusion injury group(group MIRI) and Nrf2 gene overexpression group(group Nrf2). Myocardial tissues were transfected by recombinant adenovirus vector mediated enhanced green fluorescent protein (Ad- EGFP) via coronary artery in group Sham and group MIRI, while myocardial tissues were transfected by recombinant adenovirus vector mediated human Nrf2 gene (Acl Nrf2) in group Nrf2. Myocardial ischemia reperfusion injury (or sham operation) were induced three days later. Hemodynamic parameters changes were monitored by carotid artery intubation reaching left ventricle, and the concentration of cardiac troponin I (cTnI) was detected. Results HR, LVESP and 4- dp/dt max in group MIRI and Nrf2 decreased (P 〈0.05)in the period of ischemia and repeffusion, while LVEDP increased, compared with Sham group. There were no significant differences in HR between group MIRI and group Nrf2. LVESP±dp/dt max increased significantly while LVET)P decreased significantly in group Nrf2 compared with group MIRI(P〈0. 05). At the end of the reperfusion, cTnI concentration in group MIRI and group Nrf2 were higher compared to group Sham significantly(P〈0. 05), while those in group Nrf2 were lower than group MIRI significantly(P〈0. 05). Conclusion Overexpression of Nrf2 gene in rat's myocardial tissue could improve hemodynamic disorder and inhibit the inereasement of cTnI concentration caused by myocardial ischemia-repeffusion injury.
出处 《临床麻醉学杂志》 CAS CSCD 北大核心 2013年第5期498-501,共4页 Journal of Clinical Anesthesiology
基金 长沙市科技局项目(K1005032-31)
关键词 心肌缺血-再灌注损伤 核因子-E2相关因子2 血流动力学 心肌肌钙蛋白I 氧化 应激 Myocardial ischemia reperfusion injury Nuclear factor E2 related factor2 Hemodynamics Cardiac troponin I Oxidative stress
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参考文献9

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同被引文献110

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