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虎杖苷对急性心肌梗死所致心脏损伤的保护作用 被引量:5

Protective Effect of Polydatin on Heart Injury Induced by Acute Myocardial Infarction
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摘要 为了考察虎杖苷对急性心肌梗死所致心脏损伤的保护作用,本研究对H9c2大鼠心肌细胞进行缺氧诱导来模拟急性心肌梗死中心肌细胞的变化。然后用200μmol/L的虎杖苷处理心肌细胞12 h。考察虎杖苷对心肌细胞活力、细胞凋亡及相关蛋白(caspase-3, Bcl-2)和ROS生成的应用,并用小干扰RNA敲低Nrf2,考察敲低Nrf2对心肌细胞的影响。研究显示,缺氧处理可显著降低心肌细胞活力并增加细胞凋亡率,而虎杖苷可抑制缺氧诱导的细胞活力降低和细胞凋亡。虎杖苷可显著抑制缺氧诱导的caspase-3的下调并抑制缺氧诱导的Bcl-2的上调。虎杖苷可显著抑制缺氧诱导的Nrf2和HO-1的下调。敲低Nrf2可降低H9c2心肌细胞活力并增加细胞凋亡率。敲低Nrf2可上调caspase-3表达,并下调Bcl-2和Nrf2/HO-1信号通路的表达。缺氧可诱导H9c2细胞中ROS的产量升高,虎杖苷可抑制ROS的生成。然而,敲低Nrf2可导致细胞中ROS产量再次升高。虎杖苷具有抑制缺氧诱导的心肌细胞凋亡的作用,并且虎杖苷可通过抗氧化作用来减轻急性心肌梗死所致的心脏损伤。虎杖苷的抗氧化和心肌保护作用部分依赖于Nrf2/HO-1信号通路。 To investigate the protective effect of polydatin on cardiac injury induced by acute myocardial infarction, in this study, H9 c2 rat cardiomyocytes were induced by hypoxia to simulate changes in cardiomyocytes in acute myocardial infarction. Then cardiomyocytes were treated with 200 μmol/L of polydatin for 12 h. The effects of polydatin on myocardial cell viability, apoptosis and related proteins(caspase-3, Bcl-2) and ROS production were investigated, and the effect of knockdown of Nrf2 on cardiomyocytes were investigated by transfecting small interfering RNA. Studies showed that hypoxia treatment could significantly reduce myocardial cell viability and increase apoptosis rate, while polydatin could inhibit hypoxia-induced cell viability reduction and apoptosis.Polydatin could significantly inhibit hypoxia-induced down-regulation of caspase-3 and inhibit hypoxia-induced upregulation of Bcl-2. Polydatin could significantly inhibit hypoxia-induced down-regulation of Nrf2 and HO-1.Knockdown of Nrf2 reduced H9c2 cardiomyocyte viability and increased apoptotic rate. Knockdown of Nrf2 could up-regulate caspase-3 expression and down-regulate the expression of Bcl-2 and Nrf2/HO-1 signaling pathways. Hypoxia induced an increase in ROS production in H9c2 cells, and polydatin inhibited ROS production.However, knocking down Nrf2 could lead to an increase in ROS production in cells. Polydatin has an inhibitory effect on hypoxia-induced apoptosis of cardiomyocytes, and polydatin can reduce cardiac damage caused by acute myocardial infarction through anti-oxidation. The antioxidant and myocardial protective effects of polydatin are partially dependent on the Nrf2/HO-1 signaling pathway.
作者 曾晨 黄莺 毛莉娜 Zeng Chen;Huang Ying;Mao Lina(Wuhan No.1 Hospital,Wuhan,430030)
机构地区 武汉市第一医院
出处 《基因组学与应用生物学》 CAS CSCD 北大核心 2020年第3期1362-1368,共7页 Genomics and Applied Biology
关键词 虎杖苷 急性心肌梗死 心肌细胞 氧化应激 细胞凋亡 Nrf2/HO-1 Polydatin Acute myocardial infarction Cardiomyocytes Oxidative stress Apoptosis Nrf2/HO-1
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