目的 探究大株红景天(Rhodiola wallichiana var. cholaensis, RW)总提通过调控 miR-378a-3p抑制细胞凋亡发挥保护心肌细胞缺氧/复氧损伤的作用机制。方法 本研究以RW为研究对象,利用缺氧小室建立H9C2大鼠心肌细胞缺氧(hypoxic, H)/复氧(reoxygenation, R)体外模型,通过实时荧光定量PCR法测定miR-378a-3p的表达;四甲基偶氮唑盐微量酶反应比色法(MTT)测定细胞活力;线粒体膜电位检测及免疫印迹反应等方法从细胞凋亡的角度探索RW、miR-378a-3p和H/R之间潜在的联系。结果 与H/R组相比,RW预保护后明显上调了miR-378a-3p及其靶标蛋白胰岛素样生长因子1受体(IGF1R)的表达、提高了细胞存活率和线粒体膜电位、下调了活化半胱胺酸蛋白酶-3(Cleaved-caspase3)与相关死亡促进因子(Bad)的表达。结论 RW可以通过上调miR-378a-3p进而调控IGF1R/磷脂酰肌醇3-激酶(PI3K)/丝苏氨酸激酶(Akt)信号通路发挥H/R的保护作用。
Abstract
OBJECTIVE To explore the mechanism of total extract of Rhodiola wallichiana var. cholaensis (RW) in protecting myocardial cells from hypoxia/reoxygenation injury by regulating miR-378a-3p to inhibit apoptosis. METHODS In this study, RW was used as the research object, and an in vitro model of H9C2 rat myocardial cells was established by hypoxic (H)/reoxygenation (R) chamber. The expression of miR-378a-3p was determined by real-time fluorescence quantitative PCR and cell viability was determined by MTT. Mitochondrial membrane potential detection and Western blotting were used to explore the potential relationship among RW, miR-378a-3p and cardiomyocyte hypoxia/reoxygenation injury from the perspective of cell apoptosis. RESULTS Compared with the H/R group, the expression of miR-378a-3p and its target protein IGF1R were significantly up-regulated, cell survival rate and mitochondrial membrane potential were increased, and cleaved caspase3 and bad expression were down-regulated after RW pre-protection. CONCLUSION RW plays a protective role in myocardial hypoxia/reoxygenation injury by regulating IGF1R/PI3K/Akt signaling pathway by up-regulating miR-378a-3p.
关键词
大株红景天 /
心肌缺血再灌注 /
细胞凋亡 /
miR-378a-3p
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Key words
Rhodiola wallichiana var.cholaensis /
myocardial ischemia reperfusion /
cell apoptosis /
miR-378a-3p
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中图分类号:
R966
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