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首页> 外文期刊>RSC Advances >20(S)-Ginsenoside Rg2 attenuates myocardial ischemia/reperfusion injury by reducing oxidative stress and inflammation: role of SIRT1
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20(S)-Ginsenoside Rg2 attenuates myocardial ischemia/reperfusion injury by reducing oxidative stress and inflammation: role of SIRT1

机译：20（s） - 上林苷Rg2通过减少氧化应激和炎症来衰减心肌缺血/再灌注损伤：SIRT1的作用

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Previously we demonstrated that 20(S)-ginsenoside Rg2 protects cardiomyocytes from H2O2-induced injury by inhibiting reactive oxygen species (ROS) production, increasing intracellular levels of antioxidants and attenuating apoptosis. We explored the protective effect of 20(S)-ginsenoside Rg2 on myocardial ischemia/reperfusion (MI/R) injury and to clarify its potential mechanism of action. Rats were exposed to 20(S)-ginsenoside Rg2 in the presence/absence of the silent information regulator SIRT(1) inhibitor EX527 and then subjected to MI/R. 20(S)-Ginsenoside Rg2 conferred a cardioprotective effect by improving post-ischemic cardiac function, decreasing infarct size, reducing the apoptotic index, diminishing expression of creatine kinase-MB, aspartate aminotransferase and lactate dehydrogenase in serum, upregulating expression of SIRT1, B-cell lymphoma-2, procaspase-3 and procaspase-9, and downregulating expression of Bax and acetyl (Ac)-p53. Pretreatment with 20(S)-ginsenoside Rg2 also resulted in reduced myocardial superoxide generation, gp91(phox) expression, malondialdehyde content, cardiac pro-inflammatory markers and increased myocardial activities of superoxide dismutase, catalase and glutathione peroxidase. These results suggested that MI/R-induced oxidative stress and inflammation were attenuated significantly by 20(S)-ginsenoside Rg2. However, these protective effects were blocked by EX527, indicating that SIRT1 signaling may be involved in the pharmacological action of 20(S)-ginsenoside Rg2. Our results demonstrated that 20(S)-ginsenoside Rg2 attenuates MI/R injury by reducing oxidative stress and inflammatory responses via SIRT1 signaling.
机译：以前，我们证明了20（S）-Ginsenaine RG2通过抑制反应性氧物质（ROS）产生，增加抗氧化剂和衰减细胞凋亡，保护来自H 2 O 2诱导的损伤的心肌细胞。我们探讨了20（S） - 新皂苷RG2对心肌缺血/再灌注（MI / R）损伤的保护作用，并阐明其潜在的作用机制。在静音信息调节剂SIRT（1）抑制剂EX527的存在/不存在下暴露于20（S）-Ginsenaine RG2，然后进行Mi / R。 20（S） - 甘糖苷RG2通过改善缺血性心脏功能，降低梗死指数，降低凋亡指数，捕获激酶-MB，天冬氨酸氨基转移酶和乳酸乳清氨酸脱氢酶的凋亡指数，上调表达SIRT1，B的表达-Cell淋巴瘤-2，procaspase-3和procaspase-9，以及下调Bax和乙酰基（AC）-P53的表达。用20（S） - 喹啉基RG2也导致心肌超氧化物产生降低，GP91（PHOX）表达，丙二醛含量，心脏促炎标记物，并增加超氧化物歧化酶，过氧化氢酶和谷胱甘肽过氧化物酶的增加的心肌活性。这些结果表明MI / R诱导的氧化胁迫和炎症明显衰减20（S）-Ginsenaine RG2。然而，这些保护作用被ex527阻断，表明SIRT1信号传导可以参与20（S）-Ginsenaine RG2的药理学作用。我们的结果表明，20（S） - 喹啉酯RG2通过通过SIRT1信号传导降低氧化应激和炎症反应来衰减MI / R损伤。

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  • 来源
    《RSC Advances》 |2018年第42期|共16页
  • 作者

    Fu Wenwen; Xu Huali; Yu Xiaofeng; Lyu Chen; Tian Yuan; Guo Minyu; Sun Jiao; Sui Dayun;

  • 作者单位

    Jilin Univ Sch Pharmaceut Sci Dept Pharmacol Changchun 130021 Peoples R China;

    Jilin Univ Sch Pharmaceut Sci Dept Pharmacol Changchun 130021 Peoples R China;

    Jilin Univ Sch Pharmaceut Sci Dept Pharmacol Changchun 130021 Peoples R China;

    Jilin Univ Sch Pharmaceut Sci Dept Pharmacol Changchun 130021 Peoples R China;

    Jilin Univ Sch Pharmaceut Sci Dept Pharmacol Changchun 130021 Peoples R China;

    Jilin Univ Sch Pharmaceut Sci Dept Pharmacol Changchun 130021 Peoples R China;

    Jilin Univ Sch Nursing Changchun 130021 Peoples R China;

    Jilin Univ Sch Pharmaceut Sci Dept Pharmacol Changchun 130021 Peoples R China;

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  • 中图分类 化学;
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