Ginsenoside compound-Mc1 attenuates oxidative stress and apoptosis in cardiomyocytes through an AMP-activated protein kinase-dependent mechanism
Ginsenoside compound-Mc1 attenuates oxidative stress and apoptosis in cardiomyocytes through an AMP-activated protein kinase-dependent mechanism
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DOI：
10.1016/j.jgr.2019.08.006
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发表时间：
2020-07-01
影响因子：
6.3
通讯作者：
Yoo, Hye Jin
中科院分区：
文献类型：
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作者：
Hong, So-hyeon;Hwang, Hwan-Jin;Yoo, Hye Jin
背景：人参皂苷化合物-Mc1（Mc1）是从人参提取物中获得的去糖基化人参皂苷的一员。虽然几种人参皂苷具有心脏保护作用，但这一作用尚未在人参皂苷Mc1中得到证实。方法：我们用过氧化氢(H2O2)和人参皂苷Mc1处理H9c2细胞以评估Mc1的抗氧化作用。测量抗氧化剂分子、过氧化氢酶和超氧化物歧化酶 2 (SOD2) 的水平，并使用 Bcl2 相关 X 蛋白 (Bax):B 细胞淋巴瘤 - 超大比率、细胞毒性测定和流式细胞术测定细胞活力。我们使用人参皂苷 Mc1 培育高脂饮食 (HFD) 诱导的肥胖小鼠，并评估其心脏组织，以评价人参皂苷 Mc1 的抗氧化作用和减少纤维化的能力。 结果：人参皂苷 Mc1 显着增加 H9c2 细胞中磷酸化 AMP 激活蛋白激酶 (AMPK) 的水平。人参皂苷Mc1处理后过氧化氢酶和SOD2的表达水平显着增加，导致H2O2介导的活性氧产生减少。人参皂苷 Mc1 治疗还显着降低了 H2O2 介导的 Bax:Bcl2 比率升高和 DNA 损伤细胞的数量，而 AMPK 抑制剂治疗则显着减弱了这种现象。与体外数据一致，人参皂苷 Mc1 上调 HFD 诱导的肥胖小鼠心脏组织中过氧化氢酶和 SOD2 的水平，降低 Bax:B 细胞淋巴瘤特大比值和 caspase-3 活性，导致胶原沉积减少。结论：人参皂苷 Mcl 通过 AMPK 依赖性机制降低 H9c2 细胞和从 HFD 喂养的小鼠分离的心脏组织中的氧化应激并增加细胞活力，表明其作为抗氧化药物的潜力。氧化应激相关心脏病的新型治疗剂。 (C) 2019 年韩国人参学会。 Elsevier B.V. 的出版服务
Background: Ginsenoside compound-Mc1 (Mc1) is a member of the deglycosylated ginsenosides obtained from ginseng extract. Although several ginsenosides have a cardioprotective effect, this has not been demonstrated in ginsenoside Mc1.Methods: We treated H9c2 cells with hydrogen peroxide (H2O2) and ginsenoside Mc1 to evaluate the antioxidant effects of Mc1. The levels of antioxidant molecules, catalase, and superoxide dismutase 2 (SOD2) were measured, and cell viability was determined using the Bcl2-associated X protein (Bax):B-cell lymphoma-extra large ratio, a cytotoxicity assay, and flow cytometry. We generated mice with high-fat diet (HFD)-induced obesity using ginsenoside Mc1 and assessed their heart tissues to evaluate the antioxidant effect and the fibrosis-reducing capability of ginsenoside Mc1.Results: Ginsenoside Mc1 significantly increased the level of phosphorylated AMP-activated protein kinase (AMPK) in the H9c2 cells. The expression levels of catalase and SOD2 increased significantly after treatment with ginsenoside Mc1, resulting in a decrease in the production of H2O2-mediated reactive oxygen species. Treatment with ginsenoside Mc1 also significantly reduced the H2O2-mediated elevation of the Bax:Bcl2 ratio and the number of DNA-damaged cells, which was significantly attenuated by treatment with an AMPK inhibitor. Consistent with the in vitro data, ginsenoside Mc1 upregulated the levels of catalase and SOD2 and decreased the Bax:B-cell lymphoma-extra large ratio and caspase-3 activity in the heart tissues of HFD-induced obese mice, resulting in reduced collagen deposition.Conclusion: Ginsenoside Mcl decreases oxidative stress and increases cell viability in H9c2 cells and the heart tissue isolated from HFD-fed mice via an AMPK-dependent mechanism, suggesting its potential as a novel therapeutic agent for oxidative stress-related cardiac diseases. (C) 2019 The Korean Society of Ginseng. Publishing services by Elsevier B.V.