Ischemia–reperfusion (I/R) injury is a major side effect associated with coronary heart disease (CHD). Gypenoside A (GP) is one of the dominant active components of Gynostemma pentaphyllum and has the potential to attenuate myocardial I/R injuries. The major purpose of this study was to explore the mechanism driving the protective effect of GP on myocardial tissue by focusing on the interaction between GP and miR‐143‐3p. Cardiomyocytes were pre‐treated with GP and subjected to oxygen–glucose deprivation/re‐oxygenation (OGD/R). Changes in cell viability, apoptosis, and expression levels of factors involved in the adenosine monophosphate activated protein kinase (AMPK)/Foxo1‐mediated miR‐143‐3p pathway were detected. The levels of AMPK and miR‐143‐3p were then modulated using an inhibitor and a mimic, respectively, to confirm their central roles in the effect of GP. The administration of GP attenuated OGD/R‐induced injuries by increasing cell viability and suppressing apoptosis, which was associated with the activation of AMPK/Foxo1 signaling and the decreased level of miR‐143‐3p. The down‐regulation of AMPK and up‐regulation of miR‐143‐3p both counteracted the function of GP on cardiomyocytes. The role of miR‐143‐3p suppression in the anti‐I/R effect of GP was also verified with rat model. The injection of miR‐143‐3p agomir inhibited the cardio‐protective effect of GP in a manner similar to that in the in vitro assays. Our results confirm the cardio‐protective effect of GP, which is exerted by suppressing the level of miR‐143‐3p via the activation of AMPK signaling.

中文翻译：

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绞股蓝皂苷A通过激活AMPK / Foxo1途径抑制miR-143-3p水平，从而保护缺血/再灌注损伤。

缺血再灌注（I / R）损伤是与冠心病（CHD）相关的主要副作用。绞股蓝总皂甙A（GP）是绞股蓝的主要活性成分之一并有可能减轻心肌I / R损伤。这项研究的主要目的是通过关注GP和miR-143-3p之间的相互作用来探索驱动GP对心肌组织保护作用的机制。心肌细胞用GP预处理，并进行了氧葡萄糖剥夺/再充氧（OGD / R）。检测了细胞活力，凋亡和腺苷单磷酸激活蛋白激酶（AMPK）/ Foxo1介导的miR-143-3p通路中相关因子表达水平的变化。然后分别使用抑制剂和模拟物调节AMPK和miR‐143-3p的水平，以确认它们在GP效应中的核心作用。GP的给药通过增加细胞活力并抑制细胞凋亡来减轻OGD / R诱导的损伤，这与AMPK / Foxo1信号的激活和miR‐143‐3p水平降低有关。AMPK的下调和miR-143-3p的上调均抵消了GP在心肌细胞上的功能。大鼠模型也证实了miR‐143‐3p抑制在GP的抗I / R效应中的作用。注射miR‐143‐3pagomir可抑制GP的心脏保护作用，其方式类似于体外测定。我们的结果证实了GP的心脏保护作用，这是通过激活AMPK信号来抑制miR-143-3p的水平而发挥的。大鼠模型也证实了miR‐143‐3p抑制在GP的抗I / R效应中的作用。注射miR‐143‐3pagomir可抑制GP的心脏保护作用，其方法与体外测定相似。我们的结果证实了GP的心脏保护作用，这是通过激活AMPK信号来抑制miR-143-3p的水平而发挥的。大鼠模型也证实了miR‐143‐3p抑制在GP的抗I / R效应中的作用。注射miR‐143‐3pagomir可抑制GP的心脏保护作用，其方式类似于体外测定。我们的结果证实了GP的心脏保护作用，这是通过激活AMPK信号来抑制miR-143-3p的水平而发挥的。