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首页> 外文期刊>Life sciences >Daidzein administration in vivo reduces myocardial injury in a rat ischemia/reperfusion model by inhibiting NF-kappaB activation.
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Daidzein administration in vivo reduces myocardial injury in a rat ischemia/reperfusion model by inhibiting NF-kappaB activation.

机译：通过抑制NF-κB的活化，黄豆苷元的体内给药减少了大鼠缺血/再灌注模型中的心肌损伤。

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AIMS: We tested the hypothesis that daidzein may reduce myocardial damage by both inhibiting the release of cytokines and limiting the nuclear translocation of NF-kappaB. MAIN METHODS: Male Sprague-Dawley rats were anesthetized, and the left anterior descending coronary artery (LAD) was ligated for 25 min. Twenty-four hours after reperfusion was established, the hemodynamics and infarct size were examined. KEY FINDINGS: Treatment with daidzein (10 mg/kg, i.p.) 1 h prior to the ischemia/reperfusion procedure (I/R) reduced the infarct size by 52.8% (P<0.05). Daidzein also significantly improved I/R-induced myocardial contractile dysfunction by improving the left ventricular diastolic pressure and the positive and negative maximal values of the first derivative of the left ventricular pressure. In addition, daidzein reduced the plasma levels of TNF-alpha and IL-6 in I/R rats and decreased malondialdehyde levels, myeloperoxidase activity, catalase activity and neutrophil infiltration in I/R rat myocardium.Interestingly, daidzein inhibited I/R-induced myocardial apoptosis by decreasing DNA strand breaks and cleaved caspase-3 activity. Furthermore, daidzein inhibited both the nuclear translocation of NF-kappaB in I/R rat hearts and the H(2)O(2)-induced activation of NF-kappaB-luciferase activity in human umbilical vein endothelial cells. SIGNIFICANCE: This study reveals that the administration of daidzein in vivo attenuates I/R-induced myocardial damage via inhibition of NF-kappaB activation, which in turn may suppress inflammatory cytokine expression.
机译：目的：我们测试了黄豆苷元可能通过抑制细胞因子的释放和限制NF-κB的核转运而减少心肌损伤的假说。主要方法：麻醉雄性Sprague-Dawley大鼠，结扎左冠状动脉左前降支（LAD）25分钟。建立再灌注后二十四小时，检查血流动力学和梗死面积。主要发现：在缺血/再灌注程序（I / R）前1小时，用大豆苷元（10 mg / kg，腹腔注射）治疗可将梗死面积减少52.8％（P <0.05）。大豆苷元还通过改善左心室舒张压和左心室压力一阶导数的正负最大值来显着改善I / R引起的心肌收缩功能障碍。此外，大豆苷元降低了I / R大鼠的血浆TNF-α和IL-6水平，并降低了I / R大鼠心肌中的丙二醛水平，髓过氧化物酶活性，过氧化氢酶活性和中性粒细胞浸润。有趣的是，大豆苷元抑制了I / R诱导的心肌缺血。通过减少DNA链断裂和切割caspase-3活性来减少心肌细胞凋亡。此外，黄豆苷元抑制I / R大鼠心脏中NF-kappaB的核易位和人脐静脉内皮细胞中H（2）O（2）诱导的NF-kappaB-荧光素酶活性的激活。意义：这项研究表明，通过抑制NF-κB的活化，黄豆苷元的体内给药可减轻I / R诱导的心肌损伤，进而抑制炎症性细胞因子的表达。

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