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首页> 外文期刊>RSC Advances >Vitexin mitigates myocardial ischemia reperfusion-induced damage by inhibiting excessive autophagy to suppress apoptosis via the PI3K/Akt/mTOR signaling cascade
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Vitexin mitigates myocardial ischemia reperfusion-induced damage by inhibiting excessive autophagy to suppress apoptosis via the PI3K/Akt/mTOR signaling cascade

机译：VITEXIN通过抑制过量的自噬抑制通过PI3K / AKT / MTOR信号传导级联抑制细胞凋亡来减轻心肌缺血再灌注损伤

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摘要

Myocardial ischemia reperfusion (MI/R) injury is reported to induce apoptosis and autophagy of myocardial cells and contribute to adverse cardiovascular outcomes. Vitexin, a flavonoids compound, exhibited anti-inflammatory, anti-oxidative and antitumor effects in various studies. Here, we investigated the cardioprotective effect and underlying mechanism of vitexin treatment in MI/R injury in vivo and in vitro. We found that vitexin decreased the high cell apoptosis rate caused by MI/R injury significantly in a dose-dependent manner. The expression of cleaved Caspase-3 and Bax was down-regulated and the expression of Bcl-2 was up-regulated by vitexin compared with MI/R model group, indicating that vitexin suppressed apoptosis of rat cardiomyocytes H9c2 cells in MI/R injury. The concentrations of LDH, CK and MDA were decreased while the concentration of SOD was increased by vitexin during MI/R injury. Moreover, vitexin also suppressed autophagy of H9c2 cells in MI/R injury by down-regulating the expression of Beclin1 and LC3I/II while up-regulating the expression of p62. Activation of autophagy by Rapa significantly increased cleaved Caspase-3, Bcl-2 expression and the concentration of LDH, CK, MDA while decreased the concentration of SOD, indicating that vitexin inhibited autophagy to suppress apoptosis of H9c2 cells in MI/R injury. The co-treatment of PI3K inhibitor LY294002 reversed the inhibition on apoptosis and autophagy by vitexin, suggesting that vitexin inhibited apoptosis and autophagy to ameliorate MI/R injury through activation of PI3K/Akt/mTOR signaling pathway. We also constructed MI/R animal model using C57BL/6 mice to investigate the cardioprotective effects of vitexin in vivo. We observed that vitexin mitigated MI/R injury by decreasing the concentrations of LDH, CK and MDA, increasing the concentration of SOD, and counteracting the irregular pathological changes induced by MI/R injury dose-dependently. Vitexin also suppressed apoptosis and autophagy in myocardium cells of C57BL/6 mice in MI/R injury via activation of PI3K/Akt/mTOR signaling pathway. In conclusion, vitexin mitigated MI/R injury by inhibiting apoptosis and excessive autophagy via the PI3K/Akt/mTOR signaling pathway.
机译：据报道，心肌缺血再灌注（MI / R）损伤诱导心肌细胞的凋亡和自噬，并有助于不良心血管结果。 Vitexin，一种类黄酮化合物，在各种研究中表现出抗炎，抗氧化和抗肿瘤作用。在这里，我们研究了体内和体外Mi / R损伤中Vitexin治疗的心脏保护作用和潜在机制。我们发现Vitexin以剂量依赖性方式显着降低了Mi / R损伤引起的高细胞凋亡率。将切割的Caspase-3和Bax的表达下调，与Mi / R模型组相比，Vitexin对Bcl-2的表达上调，表明Vitexin在Mi / R损伤中抑制了大鼠心肌细胞H9C2细胞的凋亡。降低LDH，CK和MDA的浓度，同时在MI / R损伤期间通过VITEXIN增加SOD的浓度。此外，通过在调节P62的表达的同时，通过降低BECLIN1和LC3I / II的表达，vitexin在MI / R损伤中抑制了H9C2细胞的自噬。通过RAPA激活自噬发生显着增加了切割的Caspase-3，Bcl-2表达和LDH，CK，MDA的浓度，同时降低了SOD的浓度，表明Vitexin抑制了抑制Mi / R损伤中H9C2细胞凋亡的凋亡。 PI3K抑制剂LY294002的共同治疗逆转了VITEXIN对细胞凋亡和自噬的抑制作用，旨在通过激活PI3K / AKT / MTOR信号通路的激活来抑制凋亡和自噬能凋亡和自噬。我们还使用C57BL / 6小鼠构建了MI / R动物模型，以研究VITEXIN在体内的心脏保护作用。我们观察到VITEXIN通过降低LDH，CK和MDA的浓度，增加SOD的浓度，并依靠依赖性损伤MI / R损伤诱导的不规则病理变化来减少MI / R损伤。通过PI3K / AKT / MTOR信号传导途径的激活，VITEXIN在MI / R损伤中抑制了C57BL / 6小鼠的心肌细胞中的细胞凋亡和自噬。总之，VITEXIN通过PI3K / AKT / MTOR信号通路抑制细胞凋亡和过度自噬而减轻了MI / R损伤。

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  • 来源
    《RSC Advances》 |2017年第89期|共11页
  • 作者

    Tang Zhaobin; Yang Lei; Zhang Xuesong;

  • 作者单位

    First Hosp Zibo Dept Cardiol Zibo 255200 Shandong Peoples R China;

    Hosp Laiwu Steel Grp Dept Cardiol Laiwu City 271100 Shandong Peoples R China;

    Liaocheng Peoples Hosp Dept Cardiol 67 Dong Chang West Rd Liaocheng 252000 Shandong Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 化学;
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