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Korean Society for Biochemistry and Molecular Biology (생화학분자생물학회)
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Celastrol suppresses expression of adhesion molecules and chemokines by inhibiting JNK-STAT1/NF-κB activation in poly(I:C)-stimulated astrocytes

  • An, Soo Yeon (Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University) ;
  • Youn, Gi Soo (Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University) ;
  • Kim, Hyejin (Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University) ;
  • Choi, Soo Young (Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University) ;
  • Park, Jinseu (Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University)
  • Received : 2016.07.18
  • Accepted : 2016.08.25
  • Published : 2017.01.31
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Abstract

In the central nervous system, viral infection can induce inflammation by up-regulating pro-inflammatory mediators that contribute to enhanced infiltration of immune cells into the central nervous areas. Celastrol is known to exert various regulatory functions, including anti-microbial activities. In this study, we investigated the regulatory effects and the mechanisms of action of celastrol against astrocytes activated with polyinosinic-polycytidylic acid (poly(I:C)), a synthetic dsRNA, as a model of pro-inflammatory mediated responses. Celastrol significantly inhibited poly(I:C)-induced expression of adhesion molecules, such as ICAM-1/VCAM-1, and chemokines, such as CCL2, CXCL8, and CXCL10, in CRT-MG human astroglioma cells. In addition, celastrol significantly suppressed poly(I:C)-induced activation of JNK MAPK and STAT1 signaling pathways. Furthermore, celastrol significantly suppressed poly(I:C)-induced activation of the $NF-{\kappa}B$ signaling pathway. These results suggest that celastrol may exert its regulatory activity by inhibiting poly(I:C)-induced expression of pro-inflammatory mediators by suppressing activation of JNK MAPK-STAT1/$NF-{\kappa}B$ in astrocytes.

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References

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