KMID : 0043320120350071259
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Archives of Pharmacal Research 2012 Volume.35 No. 7 p.1259 ~ p.1267
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The effects of ginsenoside Rb1 on JNK in oxidative injury in cardiomyocytes
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Li Jing
Shao Zuo Hui Xie Jing Tian Wang Chong Zhi Ramachandran Srinivasan Yin Jun Jie Aung Han Li Chang Qing Qin Gina Hoek Terry Vanden Yuan Chun Su
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Abstract
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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 ¥ìM) 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 ¡¾ 2.9% (n = 12, p < 0.05), 30.5 ¡¾ 5.1% (n = 12, p < 0.05) and 28.6 ¡¾ 3.1% (n = 12, p < 0.01) respectively, compared to H2O2-exposed cells (48.2 ¡¾ 3.3%, n = 12). This cardioprotective effect of gRb1 was associated with attenuated intracellular ROS generation as measured by 6-carboxy-2¡Ç, 7¡Ç-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 ¥ìM) (p < 0.01). Co-treatment of gRb1 with a specific inhibitor of JNK SP600125 (10 ¥ìM) 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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KEYWORD
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Ginsenoside Rb1, Oxidative stress, Cardiomyocyte, JNK
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