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Ginsenoside Re downregulates ICAM-1 expression, inhibits polymorphonuclear infiltration, and ameliorates ischemia-reperfusion injury

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Abstract

In this study, we investigate the effects of ginsenoside Re on the expression of intercellular adhesion molecule-1 (ICAM-1), neutrophil infiltration, and myeloperoxidase (MPO) activity during reperfusion of ischemic tissue. The model of acute ischemia reperfusion was established by ligating the left anterior descending branch of the coronary artery in Wistar rats. After ginsenoside Re administration, expression of ICAM-1 was measured by Western blotting; hematoxylin and eosin was used to analyze myocardial damage and polymorphonuclear leukocyte (PMN) infiltration. The number of PMNs per high-power field was calculated. The infarcted area and the level of MPO were also measured. This showed that ginsenoside Re administration markedly decreased the infarct size compared with that in the saline-treated I/R group (P < 0.05), significantly decreased the expression of ICAM-1 (P < 0.05) and the level of MPO (P < 0.05), and inhibited PMN infiltration (P < 0.05). In addition, a significant correlation was found between the number of PMNs infiltrating cardiac tissue and the MPO level (r = 0.981, P < 0.01).

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Authors and Affiliations

  1. First Affiliated Hospital of Nanchang University, 17 Yongwaizheng Street, 330006, Nanchang, China

    L. Jing

  2. Department of Cardiology, First Affiliated Hospital of Nanchang University, 17 Yongwaizheng Street, 330006, Nanchang, China

    M. Wang, Zeqi Zheng, J. Peng, Y. Wei & Zhenzhong Zheng

  3. Department of Cardiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 JieFang Avenue, 430030, Wuhan, China

    Z. Liu

  4. Gucheng People’s Hospital, 441700, Gucheng, Hubei, China

    X. Zou

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  1. L. Jing
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  2. M. Wang
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Correspondence to Zhenzhong Zheng.

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Jing, L., Wang, M., Zheng, Z. et al. Ginsenoside Re downregulates ICAM-1 expression, inhibits polymorphonuclear infiltration, and ameliorates ischemia-reperfusion injury. Med Chem Res 19, 962–969 (2010). https://doi.org/10.1007/s00044-009-9242-4

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  • DOI: https://doi.org/10.1007/s00044-009-9242-4

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