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首页> 外文期刊>Molecules >Clematichinenoside (AR) Attenuates Hypoxia/Reoxygenation-Induced H9c2 Cardiomyocyte Apoptosis via a Mitochondria-Mediated Signaling Pathway
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Clematichinenoside (AR) Attenuates Hypoxia/Reoxygenation-Induced H9c2 Cardiomyocyte Apoptosis via a Mitochondria-Mediated Signaling Pathway

机译：Clematichinenoside（AR）通过线粒体介导的信号通路减弱缺氧/复氧诱导的H9c2心肌细胞凋亡。

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Mitochondria-mediated cardiomyocyte apoptosis is involved in myocardial ischemia/reperfusion (MI/R) injury. Clematichinenoside (AR) is a triterpenoid saponin isolated from the roots of Clematis chinensis with antioxidant and anti-inflammatory cardioprotection effects against MI/R injury, yet the anti-apoptotic effect and underlying mechanisms of AR in MI/R injury remain unclear. We hypothesize that AR may improve mitochondrial function to inhibit MI/R-induced cardiomyocyte apoptosis. In this study, we replicated an in vitro H9c2 cardiomyocyte MI/R model by hypoxia/reoxygenation (H/R) treatment. The viability of H9c2 cardiomyocytes was determined by MTT assay; apoptosis was evaluated by flow cytometry and TUNEL experiments; mitochondrial permeability transition pore (mPTP) opening was analyzed by a calcein-cobalt quenching method; and mitochondrial membrane potential (ΔΨm) was detected by JC-1. Moreover, we used western blots to determine the mitochondrial cytochrome c translocation to cytosolic and the expression of caspase-3, Bcl-2, and Bax proteins. These results showed that the application of AR decreased the ratio of apoptosis and the extent of mPTP opening, but increased ΔΨm. AR also inhibited H/R-induced release of mitochondrial cytochrome c and decreased the expression of the caspase-3, Bax proteins. Conversely, it remarkably increased the expression of Bcl-2 protein. Taken together, these results revealed that AR protects H9c2 cardiomyocytes against H/R-induced apoptosis through mitochondrial-mediated apoptotic signaling pathway. View Full-Text
机译：线粒体介导的心肌细胞凋亡与心肌缺血/再灌注（MI / R）损伤有关。 Clematichinenoside（AR）是从铁线莲的根中分离出来的三萜皂苷，具有抗MI / R损伤的抗氧化和抗炎的心脏保护作用，但是AR在MI / R损伤中的抗凋亡作用和潜在机制尚不清楚。我们假设AR可能会改善线粒体功能，以抑制MI / R诱导的心肌细胞凋亡。在这项研究中，我们通过缺氧/复氧（H / R）处理复制了体外H9c2心肌MI / R模型。用MTT法测定H9c2心肌细胞的活力。通过流式细胞术和TUNEL实验评估细胞凋亡。通过钙黄绿素-钴淬灭法分析线粒体通透性过渡孔（mPTP）的开口。 JC-1检测线粒体膜电位（ΔΨm）。此外，我们使用蛋白质印迹来确定线粒体细胞色素c向胞质的易位以及caspase-3，Bcl-2和Bax蛋白的表达。这些结果表明，AR的应用降低了细胞凋亡率和mPTP开放程度，但是增加了Δm。 AR还抑制H / R诱导的线粒体细胞色素c释放，并降低caspase-3，Bax蛋白的表达。相反，它显着增加了Bcl-2蛋白的表达。综上所述，这些结果表明AR通过线粒体介导的凋亡信号通路保护H9c2心肌细胞免受H / R诱导的凋亡。查看全文

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