首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Qi-Shen-Yi-Qi Dripping Pills Promote Angiogenesis of Ischemic Cardiac Microvascular Endothelial Cells by Regulating MicroRNA-223-3p Expression
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Qi-Shen-Yi-Qi Dripping Pills Promote Angiogenesis of Ischemic Cardiac Microvascular Endothelial Cells by Regulating MicroRNA-223-3p Expression

机译:齐申益气滴药通过调节MicroRNA-223-3P表达来促进缺血性心血管内皮细胞的血管生成

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摘要

Traditional Chinese medicine (TCM) research shows that Qi-Shen-Yi-Qi Dripping Pills (QSYQ) can promote ischemic cardiac angiogenesis. Studies have shown that microRNAs (miRNAs) are the key component of gene regulation networks, which play a vital role in angiogenesis and cardiovascular disease. Mechanisms involving miRNA by which TCM promotes ischemic cardiac angiogenesis have not been reported. We found that microRNA-223-3p (mir-223-3p) was the core miRNA of angiogenesis of rats ischemic cardiac microvascular endothelial cells (CMECs) and inhibited angiogenesis by affecting RPS6KB1/HIF-1 alpha signal pathway in previous study. Based on the results, we observed biological characteristics and optimal dosage for QSYQ intervening in rats ischemic CMECs angiogenesis and concluded that QSYQ low-dose group had the strongest ability to promote angiogenesis of ischemic myocardium. Using miRNA chip and real-time PCR techniques in this study, we identified mir-223-3p as the pivotal miRNA in QSYQ that regulated angiogenesis of ischemic CMECs. From real-time PCR and western blot analysis, research showed that gene and protein expression of factors located RPS6KB1/HIF-1 alpha signaling pathway, including HIF-1 alpha, VEGF, MAPK, PI3K, and AKT, were significantly upregulated by QSYQ to regulate angiogenesis of ischemic CMECs. This study showed that QSYQ promote ischemic cardiac angiogenesis by downregulating mir-223-3p expression in rats ischemic CMECs.
机译:中医(TCM)研究表明,齐申益气滴药(QSYQ)可促进缺血性心肌血管生成。研究表明,MicroRNA(miRNA)是基因调控网络的关键组分,其在血管生成和心血管疾病中起着至关重要的作用。尚未报道涉及中医促进缺血性心肌血管生成的miRNA的机制。我们发现MicroRNA-223-3P(miR-223-3p)是大鼠缺血性心血管内皮细胞(CMEC)血管生成的核心生成,并通过影响先前研究中的RPS6KB1 / HIF-1α信号途径抑制血管生成。基于结果,我们观察了大鼠缺血性CMECS血管生成的QYQ干预的生物学特性和最佳剂量,结论是QSyq低剂量组具有促进缺血心肌血管生成的最强能力。在本研究中使用miRNA芯片和实时PCR技术,我们将MiR-223-3P鉴定为QSyq中的枢轴miRNA,该仪表血管生成的缺血性CMEC。从实时PCR和Western印迹分析中,研究表明,RPS6KB1 / HIF-1α信号传导途径的基因和蛋白质表达,包括HIF-1α,VEGF,MAPK,PI3K和AKT,通过QSYQ显着上调调节缺血性CMEC的血管生成。该研究表明,QSyq通过下调大鼠缺血性CMEC中的miR-223-3p表达来促进缺血性心肌血管生成。

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    Affiliated Hosp Shandong Univ Tradit Chinese Med Dept Cardiol Jinan 250011 Peoples R China;

    Jining Hosp Tradit Chinese Med Dept Cardiol Jining 272000 Peoples R China;

    Shandong Univ Tradit Chinese Med Jinan 250014 Peoples R China;

    Shandong Univ Tradit Chinese Med Jinan 250014 Peoples R China;

    Weihai Hosp Tradit Chinese Med Dept Cardiol &

    Brain Weihai 264200 Peoples R China;

    Weihai Hosp Tradit Chinese Med Dept Cardiol &

    Brain Weihai 264200 Peoples R China;

    Jining Hosp Tradit Chinese Med Dept Cardiol Jining 272000 Peoples R China;

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  • 正文语种 eng
  • 中图分类 临床医学;
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