Salvianolic acid B induced upregulation of miR-30a protects cardiac myocytes from ischemia/reperfusion injury.
Salvianolic acid B induced upregulation of miR-30a protects cardiac myocytes from ischemia/reperfusion injury.
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DOI：
10.1186/s12906-016-1275-x
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发表时间：
2016-09-01
影响因子：
--
通讯作者：
Lin R
中科院分区：
文献类型：
--
作者：
Li D;Wang J;Hou J;Fu J;Liu J;Lin R
microRNA（miRNAs）是一类新型的强有力的内源性基因表达调节因子。本研究旨在确定miR-30 a是否通过抑制自噬而参与丹参素B（Sal B）对心肌缺血-再灌注（I-R）损伤的心脏保护作用。通过I-R诱导已进行原代培养的小鼠心肌细胞，并在存在miR-30 a模拟物或miR-30 a抑制剂的情况下与Sal B（25、50、100 μM）孵育。评估miR-30 a、beclin-1、LC 3-II和p-Akt蛋白的表达、细胞活力和乳酸脱氢酶（LDH）释放。Sal B可逆转miR-30 a在I-R细胞中的表达，并呈剂量依赖性。Sal B抑制I-R心肌细胞的自噬。Sal B提高了细胞活力，降低了LDH漏出率，表明自噬抑制有利于细胞存活。用miR-30 a抑制剂敲低miR-30 a可逆转Sal B对I-R损伤的抗自噬作用。此外，我们证实了Sal B通过PI 3 K/Akt信号通路在miR-30 a介导的自噬中具有保护作用，该信号通路被PI 3 K抑制剂LY 294002废除。这些数据表明，miR-30 a通过PI 3 K/Akt信号通路参与Sal B介导的针对I-R损伤的心脏保护。本文的在线版本（doi：10.1186/s12906-016-1275-x）包含补充材料，可供授权用户使用。
MicroRNAs (miRNAs) are a novel class of powerful, endogenous regulators of gene expression. This study was designed to ascertain if miR-30a is involved in the cardioprotective actions of salvianolic acid B (Sal B) against myocardial ischemia–reperfusion (I–R) injury through suppression of autophagy. Murine myocardial cells that had undergone primary culture were induced by I–R and incubated with Sal B (25, 50, 100 μM) in the presence of a miR-30a mimic or miR-30a inhibitor. Expression of miR-30a, beclin-1, LC3-II and p-Akt protein, cell viability, and lactic acid dehydrogenase (LDH) release were assessed. miR-30a expression was down-regulated remarkably in I–R cells, and this suppression could be reversed by Sal B in a dose-dependent manner. Sal B repressed autophagy in I–R myocardial cells. Sal B improved cell viability and reduced the rate of LDH leakage, which suggested that autophagy suppression was beneficial for cell survival. Knockdown of miR-30a with a miR-30a inhibitor could reverse the anti-autophagy effect of Sal B against I–R injury. Furthermore, we confirmed that Sal B has a protective role in miR-30a-mediated autophagy through the PI3K/Akt signaling pathway, which was abrogated by the PI3K inhibitor LY294002. These data suggest that miR-30a is involved in Sal B-mediated cardioprotection against I–R injury through the PI3K/Akt signaling pathway. The online version of this article (doi:10.1186/s12906-016-1275-x) contains supplementary material, which is available to authorized users.
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