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International Journal of Molecular Medicine
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Print ISSN: 1107-3756 Online ISSN: 1791-244X
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2014-January Volume 33 Issue 1

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Article

Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms

  • Authors:
    • Xizhong Sui
    • Changqing Gao
  • View Affiliations / Copyright

    Affiliations: Department of Cardiac Surgery, The PLA General Hospital, Medical School of Chinese PLA, Beijing 100098, P.R. China
  • Pages: 227-233
    |
    Published online on: November 1, 2013
       https://doi.org/10.3892/ijmm.2013.1546
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Abstract

Huperzine A (HupA), an alkaloid used in traditional Chinese medicine and isolated from Huperzia serrata, has been shown to possess diverse biological activities. The present study was undertaken to evaluate the cardioprotective potential of HupA in myocardial ischemic damage using a rat model of acute myocardial infarction. HupA significantly diminished the infarct size and inhibited the activities of myocardial enzymes, including creatine kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin T (cTnT). A significantly reduced activity of malondialdehyde (MDA) and elevated activities of superoxide dismutase (SOD), of the non-enzymatic scavenger enzyme, glutathione (GSH), as well as of glutathione peroxidase (GSH-PX) were found in the HupA-treated groups. Furthermore, decreased protein levels of caspase-3 and Bax, and increased levels of Bcl-2 were observed in the infarcted hearts of the rats treated with various concentrations of HupA. In addition, treatment with HupA markedly inhibited the expression of the nuclear factor-κB (NF-κB) subunit p65, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). These findings suggest that the cardioprotective potential of HupA is associated with its antioxidant, anti-apoptotic and anti-inflammatory properties in acute myocardial infarction in rats.
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Copy and paste a formatted citation
Spandidos Publications style
Sui X and Gao C: Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms. Int J Mol Med 33: 227-233, 2014.
APA
Sui, X., & Gao, C. (2014). Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms. International Journal of Molecular Medicine, 33, 227-233. https://doi.org/10.3892/ijmm.2013.1546
MLA
Sui, X., Gao, C."Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms". International Journal of Molecular Medicine 33.1 (2014): 227-233.
Chicago
Sui, X., Gao, C."Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms". International Journal of Molecular Medicine 33, no. 1 (2014): 227-233. https://doi.org/10.3892/ijmm.2013.1546
Copy and paste a formatted citation
x
Spandidos Publications style
Sui X and Gao C: Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms. Int J Mol Med 33: 227-233, 2014.
APA
Sui, X., & Gao, C. (2014). Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms. International Journal of Molecular Medicine, 33, 227-233. https://doi.org/10.3892/ijmm.2013.1546
MLA
Sui, X., Gao, C."Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms". International Journal of Molecular Medicine 33.1 (2014): 227-233.
Chicago
Sui, X., Gao, C."Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti-inflammatory mechanisms". International Journal of Molecular Medicine 33, no. 1 (2014): 227-233. https://doi.org/10.3892/ijmm.2013.1546
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