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Article

Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways

  • Authors:
    • Chang Chen
    • Ping Du
    • Junjie Wang
  • View Affiliations / Copyright

    Affiliations: Department of Emergency, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, P.R. China, Department of Cardiology, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, P.R. China
  • Pages: 3937-3943
    |
    Published online on: May 28, 2015
       https://doi.org/10.3892/mmr.2015.3870
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Abstract

Paeoniflorin (PF) is the main active component of the commonly used Traditional Chinese Medicine peony, Paeonia Suffruticosa. PF has diverse biological functions and exhibits anti‑oxidative, anti‑inflammatory and anti‑apoptotic activity. Inducible nitric oxide synthase (iNOS) is a catalyzing enzyme that is involved in the synthesis of nitric oxide (NO). NO has an important regulatory role in the cardiovascular, immune and nervous systems. PF has previously been demonstrated to inhibit the gene expression of iNOS. The present study aimed to identify a potentially novel cytoprotective function of PF, and to elucidate its effects against myocardial ischemic damage in a rat model of acute myocardial infarction (AMI). PF was able to significantly decrease the myocardial infarct size as well as the activities of creatine kinase (CK), the MB isoenzyme of CK, lactate dehydrogenase and cardiac troponin T. In addition, in the PF‑treated groups, the expression levels of tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and nuclear factor‑κB were markedly inhibited. Furthermore, treatment with PF inhibited the activities and protein expression levels of iNOS. Decreased caspase‑3 and caspase‑9 activities were also observed in the AMI rat model treated with various doses of PF. The results of the present study indicated that the cardioprotective effects of PF may be associated with the inhibition of inflammation and iNOS signaling pathways.
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Copy and paste a formatted citation
Spandidos Publications style
Chen C, Du P and Wang J: Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways. Mol Med Rep 12: 3937-3943, 2015.
APA
Chen, C., Du, P., & Wang, J. (2015). Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways. Molecular Medicine Reports, 12, 3937-3943. https://doi.org/10.3892/mmr.2015.3870
MLA
Chen, C., Du, P., Wang, J."Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways". Molecular Medicine Reports 12.3 (2015): 3937-3943.
Chicago
Chen, C., Du, P., Wang, J."Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways". Molecular Medicine Reports 12, no. 3 (2015): 3937-3943. https://doi.org/10.3892/mmr.2015.3870
Copy and paste a formatted citation
x
Spandidos Publications style
Chen C, Du P and Wang J: Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways. Mol Med Rep 12: 3937-3943, 2015.
APA
Chen, C., Du, P., & Wang, J. (2015). Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways. Molecular Medicine Reports, 12, 3937-3943. https://doi.org/10.3892/mmr.2015.3870
MLA
Chen, C., Du, P., Wang, J."Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways". Molecular Medicine Reports 12.3 (2015): 3937-3943.
Chicago
Chen, C., Du, P., Wang, J."Paeoniflorin ameliorates acute myocardial infarction of rats by inhibiting inflammation and inducible nitric oxide synthase signaling pathways". Molecular Medicine Reports 12, no. 3 (2015): 3937-3943. https://doi.org/10.3892/mmr.2015.3870
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