Journal
INFLAMMATION RESEARCH
Volume 59, Issue 10, Pages 809-816Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00011-010-0192-6
Keywords
Dipyrithione; Interferon-gamma; IP-10/CXCL10; JAK/STAT1 signaling; RAW264.7 cells
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Funding
- National Nature Science Foundation of China [30770842, 30771979]
- Jiangsu Major Nature Science Foundation of High Education [07KJA18026]
- Specialized Research Fund for the Doctoral Program of Higher Education of China [2007104SBJ0152]
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This study investigates the effects of dipyrithione (PTS2) on the expression of IP-10/CXCL10, which has been observed in a wide variety of chronic inflammatory disorders and autoimmune conditions. RAW264.7 cells (a murine macrophage-like cell line) were cultured in the absence or in the presence of PTS2 (3-10 mu M) together with or without IFN-gamma (10 ng/ml). IP-10/CXCL10 expression was measured by specific enzyme-amplified immunoassays and reverse transcriptase-PCR (RT-PCR). Phosphorylation of JAK1, JAK2 and STAT1 were detected by Western blot analysis. We found that PTS2 inhibited IFN-gamma-induced up-regulation of IP-10/CXCL10 protein level in a dose- and time-dependent manner in RAW264.7 cells. RT-PCR experiments showed that PTS2 suppressed IFN-gamma-induced IP-10/CXCL10 expression at mRNA levels. Mechanistically, PTS2 prevented phosphorylation of JAK1, JAK2 and STAT1, but did not interfere with the p38 pathway. Furthermore, the inhibitory effect of PTS2 on IP-10/CXCL10 up-regulation was slightly stronger than JAK2 inhibitor AG490. PTS2 inhibits IFN-gamma-induced IP-10/CXCL10 expression in RAW264.7 cells by targeting the JAK/STAT1 signaling pathway, suggesting that PTS2 could exert anti-inflammatory effects through attenuating the formation of chemokine IP-10/CXCL10.
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