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Article Open Access

YC‑1 reduces inflammatory responses by inhibiting nuclear factor‑κB translocation in mice subjected to transient focal cerebral ischemia

  • Authors:
    • Wei‑Ting Lee
    • Shih‑Huang Tai
    • Yu‑Wen Lin
    • Tian‑Shung Wu
    • E‑Jian Lee
  • View Affiliations / Copyright

    Affiliations: Institute of Biotechnology and Clinical Medicine, National Cheng Kung University, Tainan 70101, Taiwan, R.O.C., Neurophysiology Laboratory, Neurosurgical Service, Department of Surgery, National Cheng Kung University Medical Center and Medical School, Tainan 70428, Taiwan, R.O.C.
    Copyright: © Lee et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2043-2051
    |
    Published online on: June 15, 2018
       https://doi.org/10.3892/mmr.2018.9178
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Abstract

3‑(5‑hydroxymethyl‑2‑furyl)‑1‑benzyl‑indazole (YC‑1) is understood to protect against ischemic stroke, but the molecular basis for its neuroprotection remains to be fully characterized. The present study investigated the influence of YC‑1 on inflammatory responses following experimental stroke. Previous studies indicated that nuclear factor (NF)‑κB‑driven signals serve a pivotal role in mediating inflammatory responses following stroke. Ischemic stroke results in activation of NF‑κB to induce gene expression of factors including inducible nitric oxide synthase, interleukin (IL)‑1β, IL‑6 and matrix metalloproteinases (MMPs). The results of the present study demonstrated that YC‑1 effectively reduced brain infarction and brain edema, and improved blood‑brain barrier leakage. Additionally, animals treated with YC‑1 exhibited significant reductions in neutrophil and macrophage infiltration into the ischemic brain. Furthermore, YC‑1 effectively inhibited NF‑κB translocation and binding activity, and the activity and expression of MMP‑9 following ischemic stroke. In conclusion, YC‑1 may effectively attenuate NF‑κB‑induced inflammatory damage following cerebral ischemia‑reperfusion.
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Copy and paste a formatted citation
Spandidos Publications style
Lee WT, Tai SH, Lin YW, Wu TS and Lee EJ: YC‑1 reduces inflammatory responses by inhibiting nuclear factor‑κB translocation in mice subjected to transient focal cerebral ischemia. Mol Med Rep 18: 2043-2051, 2018.
APA
Lee, W., Tai, S., Lin, Y., Wu, T., & Lee, E. (2018). YC‑1 reduces inflammatory responses by inhibiting nuclear factor‑κB translocation in mice subjected to transient focal cerebral ischemia. Molecular Medicine Reports, 18, 2043-2051. https://doi.org/10.3892/mmr.2018.9178
MLA
Lee, W., Tai, S., Lin, Y., Wu, T., Lee, E."YC‑1 reduces inflammatory responses by inhibiting nuclear factor‑κB translocation in mice subjected to transient focal cerebral ischemia". Molecular Medicine Reports 18.2 (2018): 2043-2051.
Chicago
Lee, W., Tai, S., Lin, Y., Wu, T., Lee, E."YC‑1 reduces inflammatory responses by inhibiting nuclear factor‑κB translocation in mice subjected to transient focal cerebral ischemia". Molecular Medicine Reports 18, no. 2 (2018): 2043-2051. https://doi.org/10.3892/mmr.2018.9178
Copy and paste a formatted citation
x
Spandidos Publications style
Lee WT, Tai SH, Lin YW, Wu TS and Lee EJ: YC‑1 reduces inflammatory responses by inhibiting nuclear factor‑κB translocation in mice subjected to transient focal cerebral ischemia. Mol Med Rep 18: 2043-2051, 2018.
APA
Lee, W., Tai, S., Lin, Y., Wu, T., & Lee, E. (2018). YC‑1 reduces inflammatory responses by inhibiting nuclear factor‑κB translocation in mice subjected to transient focal cerebral ischemia. Molecular Medicine Reports, 18, 2043-2051. https://doi.org/10.3892/mmr.2018.9178
MLA
Lee, W., Tai, S., Lin, Y., Wu, T., Lee, E."YC‑1 reduces inflammatory responses by inhibiting nuclear factor‑κB translocation in mice subjected to transient focal cerebral ischemia". Molecular Medicine Reports 18.2 (2018): 2043-2051.
Chicago
Lee, W., Tai, S., Lin, Y., Wu, T., Lee, E."YC‑1 reduces inflammatory responses by inhibiting nuclear factor‑κB translocation in mice subjected to transient focal cerebral ischemia". Molecular Medicine Reports 18, no. 2 (2018): 2043-2051. https://doi.org/10.3892/mmr.2018.9178
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