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Article

Oxysophoridine attenuates the injury caused by acute myocardial infarction in rats through anti‑oxidative, anti‑inflammatory and anti‑apoptotic pathways

  • Authors:
    • Cong Meng
    • Chuan Liu
    • Yuanwei Liu
    • Fan Wu
  • View Affiliations / Copyright

    Affiliations: Department of Radiology, Huangdao Branch of the Affiliated Hospital of Qingdao University, Qingdao, Shandong 266555, P.R. China, Department of Clinical Medicine, Yantai Campus, Binzhou Medical University, Yantai, Shandong 264000, P.R. China, Department of Pediatrics, Dongying Hospital of Shandong Provincial Hospital, Dongying, Shandong 257091, P.R. China
  • Pages: 527-532
    |
    Published online on: October 22, 2014
       https://doi.org/10.3892/mmr.2014.2748
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Abstract

Oxysophoridine (OSR), a natural alkaloid derived from the traditional Chinese medicinal plant sophora alopecuroides, can perform a variety of pharmacological actions. The aim of the present study was to assess the cardioprotective effect of OSR against acute myocardial infarction (AMI) in rats. OSR markedly reduced infarction size and levels of specific myocardial enzymes, including creatine kinase, the MB isoenzyme of creatine kinase, lactate dehydrogenase and cardiac troponin T. A reduced level of malondialdehyde was observed, and elevated catalase, Cu/Zn‑superoxide dismutase (SOD), Mn‑SOD, non‑enzymatic scavenger glutathione and glutathione peroxidase activity were also identified in the OSR‑treated rats. Additionally, OSR inhibited the activities of various inflammatory cytokines in a dose‑dependent manner. These included nuclear factor‑κB p65, tumor necrosis factor‑α, and interleukin‑1β, ‑6 and ‑10. Furthermore, OSR treatment suppressed caspase‑3 activity in a dose‑dependent manner. These results demonstrate that OSR ameliorates cardiac damage in a rat model of AMI and that this cardioprotection may be linked with its anti‑oxidative, anti‑apoptotic and anti‑inflammatory properties.
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Copy and paste a formatted citation
Spandidos Publications style
Meng C, Liu C, Liu Y and Wu F: Oxysophoridine attenuates the injury caused by acute myocardial infarction in rats through anti‑oxidative, anti‑inflammatory and anti‑apoptotic pathways. Mol Med Rep 11: 527-532, 2015.
APA
Meng, C., Liu, C., Liu, Y., & Wu, F. (2015). Oxysophoridine attenuates the injury caused by acute myocardial infarction in rats through anti‑oxidative, anti‑inflammatory and anti‑apoptotic pathways. Molecular Medicine Reports, 11, 527-532. https://doi.org/10.3892/mmr.2014.2748
MLA
Meng, C., Liu, C., Liu, Y., Wu, F."Oxysophoridine attenuates the injury caused by acute myocardial infarction in rats through anti‑oxidative, anti‑inflammatory and anti‑apoptotic pathways". Molecular Medicine Reports 11.1 (2015): 527-532.
Chicago
Meng, C., Liu, C., Liu, Y., Wu, F."Oxysophoridine attenuates the injury caused by acute myocardial infarction in rats through anti‑oxidative, anti‑inflammatory and anti‑apoptotic pathways". Molecular Medicine Reports 11, no. 1 (2015): 527-532. https://doi.org/10.3892/mmr.2014.2748
Copy and paste a formatted citation
x
Spandidos Publications style
Meng C, Liu C, Liu Y and Wu F: Oxysophoridine attenuates the injury caused by acute myocardial infarction in rats through anti‑oxidative, anti‑inflammatory and anti‑apoptotic pathways. Mol Med Rep 11: 527-532, 2015.
APA
Meng, C., Liu, C., Liu, Y., & Wu, F. (2015). Oxysophoridine attenuates the injury caused by acute myocardial infarction in rats through anti‑oxidative, anti‑inflammatory and anti‑apoptotic pathways. Molecular Medicine Reports, 11, 527-532. https://doi.org/10.3892/mmr.2014.2748
MLA
Meng, C., Liu, C., Liu, Y., Wu, F."Oxysophoridine attenuates the injury caused by acute myocardial infarction in rats through anti‑oxidative, anti‑inflammatory and anti‑apoptotic pathways". Molecular Medicine Reports 11.1 (2015): 527-532.
Chicago
Meng, C., Liu, C., Liu, Y., Wu, F."Oxysophoridine attenuates the injury caused by acute myocardial infarction in rats through anti‑oxidative, anti‑inflammatory and anti‑apoptotic pathways". Molecular Medicine Reports 11, no. 1 (2015): 527-532. https://doi.org/10.3892/mmr.2014.2748
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