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首页> 外文期刊>Life sciences >Salidroside and tyrosol from Rhodiola protect H9c2 cells from ischemia/reperfusion-induced apoptosis
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Salidroside and tyrosol from Rhodiola protect H9c2 cells from ischemia/reperfusion-induced apoptosis

机译：红景天的红景天苷和酪醇保护H9c2细胞免受缺血/再灌注诱导的凋亡

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Aims: Heart disease is the leading cause of death worldwide. Ischemia-reperfusion injury can lead to apoptotic death of heart cells and subsequently heart failure. Rhodiola is an herbal medicine with two main bioactive compounds - salidroside (SAL) and tyrosol (TYR). This study aimed to investigate whether these two compounds can prevent ischemia/reperfusion-induced apoptosis in H9c2 cells. Main methods: Assays for total phenolics assay and Oxygen Radical Absorbance Capacity showed high antioxidant capacity of SAL and TYR. H9c2 cells were subjected to simulated ischemia/reperfusion (IR) in the presence and absence of SAL and/or TYR, and nuclei condensation, caspase-3 activity, cytochrome c release and JNK phosphorylation were determined. Key findings: In H9c2 cells, IR can lead to a 5-fold increase in p-JNK level. Apoptotic nuclei condensation, caspase-3 activity and cytochrome c release were markedly elevated, indicating the occurrence of apoptosis. SAL and TYR caused a dose-dependent inhibition of nuclear condensation. Furthermore, SAL and TYR, separately and in combination, significantly reduced caspase-3 activity, cytochrome c release and JNK activation. The anti-apoptotic effect of the combination was markedly higher than that of SAL or TYR alone. Significance: The inhibition of the JNK signaling pathway is the key mechanism for the cytoprotective effect of SAL and TYR in IR-induced apoptosis.
机译：目的：心脏病是世界范围内主要的死亡原因。缺血再灌注损伤可导致心脏细胞凋亡性死亡，进而导致心力衰竭。红景天是一种具有两种主要生物活性化合物的草药-红景天苷（SAL）和酪醇（TYR）。这项研究旨在调查这两种化合物是否可以预防缺血/再灌注诱导的H9c2细胞凋亡。主要方法：总酚含量测定和氧自由基吸收容量测定均显示出SAL和TYR的高抗氧化能力。在存在和不存在SAL和/或TYR的情况下，对H9c2细胞进行模拟的缺血/再灌注（IR），并测定细胞核浓缩，caspase-3活性，细胞色素c释放和JNK磷酸化。关键发现：在H9c2细胞中，IR可使p-JNK水平提高5倍。凋亡核浓缩，caspase-3活性和细胞色素c的释放明显升高，表明发生了凋亡。 SAL和TYR引起剂量依赖性的核浓缩抑制作用。此外，SAL和TYR分别或组合使用可显着降低caspase-3活性，细胞色素c释放和JNK激活。该组合的抗凋亡作用明显高于单独的SAL或TYR。意义：抑制JNK信号通路是SAL和TYR在IR诱导的细胞凋亡中具有细胞保护作用的关键机制。

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