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Celastrol suppresses expression of adhesion molecules and chemokines by inhibiting JNK-STAT1/NF-リB activation in poly(I:C)-stimulated astrocytes
Soo Yeon An1, Gi Soo Youn1, Hyejin Kim1, Soo Young Choi1, Jinseu Park1,*
1Department of Biological Science, Hallym University
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-リ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-リB in astrocytes.
Abstract, Accepted Manuscript(in press) [Submitted on July 18, 2016, Accepted on August 25, 2016]
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