Seselin ameliorates inflammation via targeting Jak2 to suppress the proinflammatory phenotype of macrophage.
Authors of this article are:
Feng L, Sun Y, Song P, Xu L, Wu X, Wu X, Shen Y, Sun Y, Kong L, Wu X, Xu Q.
A summary of the article is shown below:
BACKGROUND AND PURPOSE: Sepsis is a serious clinical condition with high mortality rate. Emerging evidence proved that inhibition of inflammation was beneficial for the treatment of sepsis. Here, we evaluated the anti-inflammation activity of seselin in septic mice and further detected underlying molecular mechanism.EXPERIMENTAL APPROACH: The in vivo therapeutic effect of seselin was evaluated in septic C57BL/6 mice. Sepsis was induced by cecal ligation and puncture or injection of LPS. The in virto anti-inflammation activity of seselin was determined in LPS and IFN-γ stimulated macrophages. The mechanism was investigated by co-immunoprecipitation, cellular thermal shift assay and molecular docking.KEY RESULTS: In vivo study showed that seselin obviously ameliorated cecal ligation and puncture induced sepsis in mice. In septic mice lung tissue and cultured macrophages, seselin downregulated level of pro-inflammatory factors and activity of STAT1 and p65, the master signal pathway molecules for proinflammatory macrophages polarization. Importantly, adoptive transferred with seselin pretreated BMDM significantly descended system proinflammatory factors in LPS challenged mice. The further mechanism was that seselin targeted Jak2 to block interaction with IFNγR and downstream STAT1.CONCLUSION AND IMPLICATIONS: Our study suggested the anti-inflammatory activity of seselin and identified its molecular target, Jak2. These results indicated the potential possibility of seselin in treatment of inflammatory disease via blocking the proinflammatory phenotype of macrophages.This article is protected by copyright. All rights reserved.
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