YC-1 reduces inflammatory responses by inhibiting nuclear factor-?B translocation in mice subjected to transient focal cerebral ischemia

Wei Ting Lee, Shih Huang Tai, Yu Wen Lin, Tian Shung Wu, E. Jian Lee

Research output: Contribution to journalArticle

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)-?B-driven signals serve a pivotal role in mediating inflammatory responses following stroke. Ischemic stroke results in activation of NF-?B to induce gene expression of factors including inducible nitric oxide synthase, interleukin (IL)-1ß, 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-?B translocation and binding activity, and the activity and expression of MMP-9 following ischemic stroke. In conclusion, YC-1 may effectively attenuate NF-?B-induced inflammatory damage following cerebral ischemia-reperfusion.

Original languageEnglish
Pages (from-to)2043-2051
Number of pages9
JournalMolecular Medicine Reports
Volume18
Issue number2
DOIs
Publication statusPublished - 2018 Aug

Fingerprint

Transient Ischemic Attack
Brain
Stroke
Indazoles
Macrophages
Matrix Metalloproteinase 9
Nitric Oxide Synthase Type II
Matrix Metalloproteinases
Interleukin-1
Infiltration
Gene expression
Interleukin-6
Animals
Brain Infarction
Chemical activation
Neutrophil Infiltration
Brain Edema
Brain Ischemia
Blood-Brain Barrier
Reperfusion

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Oncology
  • Cancer Research

Cite this

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title = "YC-1 reduces inflammatory responses by inhibiting nuclear factor-?B translocation in mice subjected to transient focal cerebral ischemia",
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)-?B-driven signals serve a pivotal role in mediating inflammatory responses following stroke. Ischemic stroke results in activation of NF-?B to induce gene expression of factors including inducible nitric oxide synthase, interleukin (IL)-1{\ss}, 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-?B translocation and binding activity, and the activity and expression of MMP-9 following ischemic stroke. In conclusion, YC-1 may effectively attenuate NF-?B-induced inflammatory damage following cerebral ischemia-reperfusion.",
author = "Lee, {Wei Ting} and Tai, {Shih Huang} and Lin, {Yu Wen} and Wu, {Tian Shung} and Lee, {E. Jian}",
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YC-1 reduces inflammatory responses by inhibiting nuclear factor-?B translocation in mice subjected to transient focal cerebral ischemia. / Lee, Wei Ting; Tai, Shih Huang; Lin, Yu Wen; Wu, Tian Shung; Lee, E. Jian.

In: Molecular Medicine Reports, Vol. 18, No. 2, 08.2018, p. 2043-2051.

Research output: Contribution to journalArticle

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AU - Lee, Wei Ting

AU - Tai, Shih Huang

AU - Lin, Yu Wen

AU - Wu, Tian Shung

AU - Lee, E. Jian

PY - 2018/8

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AB - 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)-?B-driven signals serve a pivotal role in mediating inflammatory responses following stroke. Ischemic stroke results in activation of NF-?B to induce gene expression of factors including inducible nitric oxide synthase, interleukin (IL)-1ß, 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-?B translocation and binding activity, and the activity and expression of MMP-9 following ischemic stroke. In conclusion, YC-1 may effectively attenuate NF-?B-induced inflammatory damage following cerebral ischemia-reperfusion.

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