The effects of ginsenoside Rb1 on JNK in oxidative injury in cardiomyocytes.
The effects of ginsenoside Rb1 on JNK in oxidative injury in cardiomyocytes.
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DOI：
10.1007/s12272-012-0717-3
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发表时间：
2012-07
影响因子：
6.7
通讯作者：
Yuan, Chun-Su
中科院分区：
文献类型：
--
作者：
Li, Jing;Shao, Zuo-Hui;Xie, Jing-Tian;Wang, Chong-Zhi;Ramachandran, Srinivasan;Yin, Jun-Jie;Aung, Han;Li, Chang-Qing;Qin, Gina;Vanden Hoek, Terry;Yuan, Chun-Su
活性氧（ROS）可通过铁相互作用（即芬顿化学和羟基自由基形成）诱导氧化损伤。我们先前的工作表明，西洋参浆果提取物和西洋参Re对氧化应激具有高度的心脏保护作用。为了扩展这项研究，我们评估了原人参二醇型人参皂苷Rb 1（gRb 1）对H2 O2诱导的心肌细胞氧化损伤的保护作用，并探讨了ROS介导的细胞内信号转导机制。使用培养的鸡胚心肌细胞（4-5天）。通过碘化丙啶和乳酸脱氢酶释放评估细胞死亡。gRb 1预处理（0.01、0.1或1 μM）处理2 h，同时用H2 O2处理（0.5 mM）处理2 h导致细胞死亡的剂量依赖性减少，36.6 ± 2.9%（n = 12，p < 0.05）、30.5 ± 5.1%（n = 12，p < 0.05）和28.6 ± 3.1%（n = 12，p < 0.01），相比于H2 O2暴露的细胞（48.2 ± 3.3%，n = 12）。gRb 1的这种心脏保护作用与6-羧基-2 ′，7′-二氯二氢荧光素二乙酸酯测定的细胞内ROS生成减弱有关，并使用JC-1测定的线粒体膜电位保持不变。ESR研究表明，gRb 1具有清除DPPH自由基和羟自由基的活性。此外，我们的数据显示，在H2 O2暴露的细胞中，JNK磷酸化（p-JNK）的增加被gRb 1（1 μM）预处理所抑制（p < 0.01）。gRb 1与JNK特异性抑制剂SP 600125（10 μM）共同处理进一步降低了p-JNK，并增强了H2 O2暴露后的细胞存活。总的来说，我们的研究结果表明，gRb 1赋予心脏保护，通过衰减ROS和抑制ROS诱导的JNK激活介导。
Reactive oxygen species (ROS) can induce oxidative injury via iron interactions (i.e. Fenton chemistry and hydroxyl radical formation). Our prior work suggested that American ginseng berry extract and ginsenoside Re were highly cardioprotective against oxidant stress. To extend this study, we evaluated the protective effect of protopanaxadiol-type ginsenoside Rb1 (gRb1) on H2O2-induced oxidative injury in cardiomyocytes and explored the ROS-mediated intracellular signaling mechanism. Cultured embryonic chick cardiomyocytes (4–5 day) were used. Cell death was assessed by propidium iodide and lactate dehydrogenase release. Pretreatment with gRb1 (0.01, 0.1, or 1 μM) for 2 h and concurrent treatment with H2O2 (0.5 mM) for 2 h resulted in a dose-dependent reduction of cell death, 36.6 ± 2.9% (n = 12, p < 0.05), 30.5 ± 5.1% (n = 12, p < 0.05) and 28.6 ± 3.1% (n = 12, p < 0.01) respectively, compared to H2O2-exposed cells (48.2 ± 3.3%, n = 12). This cardioprotective effect of gRb1 was associated with attenuated intracellular ROS generation as measured by 6-carboxy-2′, 7′-dichlorodihydrofluorescein diacetate, preserved the mitochondrial membrane potential as determined using JC-1. In the ESR study, gRb1 exhibited the scavenging DPPH and hydroxyl radical activities. Furthermore, our data showed the increased JNK phosphorylation (p-JNK) in H2O2-exposed cells was suppressed by the pretreatment with gRb 1 (1 μM) (p < 0.01). Co-treatment of gRb1 with a specific inhibitor of JNK SP600125 (10 μM) further reduced the p-JNK and enhanced the cell survival after H2O2 exposure. Collectively, our results suggest that gRb1 conferred cardioprotection that was mediated via attenuating ROS and suppressing ROS-induced JNK activation.
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影响因子：
7.4
作者：
Barbouti, A;Doulias, PT;Galaris, D
通讯作者：
Galaris, D
DOI：
10.1073/pnas.251194298
发表时间：
2001-11-20
影响因子：
11.1
作者：
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通讯作者：
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作者：
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影响因子：
5
作者：
Das, Samarjit;Otani, Hajime;Das, Dipak K.
通讯作者：
Das, Dipak K.