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Oxypaeoniflorin improves myocardial ischemia/reperfusion injury by activating the Sirt1/Foxo1 signaling pathway.

氧化芍药苷通过激活 Sirt1/Foxo1 信号通路改善心肌缺血/再灌注损伤。

  • 影响因子:1.68
  • DOI:10.18388/abp.2020_5206
  • 作者列表:"Wang K","Hu W
  • 发表时间:2020-06-18
Abstract

Myocardial ischemia/reperfusion (MI/R) injury is a leading cause of damage to cardiac tissues and is associated with high mortality and disability rates worldwide. Oxypaeoniflorin (OPA) has been found to be the main constituent of Paeonia veitchii Lynch. This study was conducted to explore the effect of OPA on MI/R injury and its potential mechanism. An in vivo MI/R injury model was established by transient coronary ligation in BALB/c mice, and an in vitro hypoxia/reoxygenation (H/R) injury model was established with rat cardiomyocyte H9c2 cells. Echocardiographic assessments demonstrated that OPA significantly reduced disruption of cardiac function and improved the indicators of ejection fraction (EF) and fractional shortening (FS). The enzyme-linked immunosorbent assay (ELISA) results suggested that OPA significantly reduced the release of myocardial infarction-related factors, such as the creatine kinase (CK-MB), cardiac troponin I (cTnI) and cardiac troponin T (cTnT). Additionally, hematoxylin-eosin (HandE) staining demonstrated that OPA markedly inhibited the myocardial apoptosis and necrosis caused by MI/R. Consistently, the results obtained from the cell counting kit-8 (CCK-8) and flow cytometry assays revealed that OPA obviously reversed the H/R-induced decrease in cell activity and increase in apoptosis of H9c2 cells. Furthermore, western blot assays indicated that OPA inhibited apoptosis by activating the Sirt1 (silent information regulator factor 2 related enzyme 1)/Foxo1(forkhead transcription factor FKHR) signaling pathway in myocardial tissues and H9c2 cells. Collectively, these novel findings are the first to provide strong evidence that OPA attenuates MI/R injury by activating the Sirt1 (silent information regulator factor 2 related enzyme 1)/Foxo1(forkhead transcription factor FKHR) signaling-mediated anti-apoptotic pathway.

摘要

心肌缺血/再灌注 (MI/R) 损伤是心脏组织损伤的主要原因,与全球高死亡率和致残率相关。已发现氧化芍药内酯苷 (OPA) 是芍药林奇的主要成分。本研究旨在探讨 OPA 对 MI/R 损伤的影响及其潜在机制。通过 BALB/c 小鼠短暂冠脉结扎建立体内 MI/R 损伤模型,体外缺氧/复氧 (H/R) 用大鼠心肌细胞 H9c2 建立损伤模型。超声心动图评估表明,OPA 显著降低了心功能的破坏,改善了射血分数 (EF) 和缩短分数 (FS) 的指标。酶联免疫吸附试验 (ELISA) 结果提示,OPA 显著减少心肌梗死相关因子的释放,如肌酸激酶 (CK-MB) 、心肌肌钙蛋白 I (cTnI) 和心肌肌钙蛋白 T (cTnT)。此外,苏木精-伊红 (HandE) 染色显示 OPA 明显抑制 MI/R 引起的心肌细胞凋亡和坏死。一致地,从细胞计数试剂盒-8 (CCK-8) 获得的结果流式细胞仪检测发现,OPA 明显逆转了 H/R 诱导的 H9c2 细胞活性降低和凋亡增加。此外,western blot 检测表明,OPA 通过激活 Sirt1 (沉默信息调节因子 2 相关酶 1)/Foxo1 (叉头转录因子 FKHR) 抑制细胞凋亡心肌组织和 H9c2 细胞中的信号通路。总的来说,这些新发现首次提供了强有力的证据,证明 OPA 通过激活 Sirt1 (沉默信息调节因子 2 相关酶 1) 来减弱 MI/R 损伤/Foxo1 (叉头转录因子 FKHR) 信号介导的抗凋亡通路。

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影响因子:2.3490
发表时间:2020-01-21
DOI:10.3389/fped.2019.00567
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影响因子:8.02
发表时间:2020-01-19
来源期刊:Genome Medicine
DOI:10.1186/s13073-019-0709-8
作者列表:["Cigdem Sevim Bayrak","Peng Zhang","Martin Tristani-Firouzi","Bruce D. Gelb","Yuval Itan"]

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