A Benzenediamine Analog FC-99 promotes M2 macrophage polarization.

What is it about?

FC-99 (N1-[(4-methoxy)methyl],-4-methyl-1,2-benzenediamine) was a benzenediamine analog synthesized in our lab. In the previous studies, FC-99 displayed an anti-inflammatory effect and a therapeutic potential on experimental sepsis. It further inhibited the LPS-induced phosphorylation of NF-κB, which were associated with M1 macrophage polarization. However, whether FC-99 directly modulates the M1/M2 polarization and the underlying mechanism of action remains unknown. Herein, this paper suggests that FC-99 could modulate macrophage polarization and is a possible therapeutic candidate for acute sepsis-induced liver injury.

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Photo by Christian Widell on Unsplash

Photo by Christian Widell on Unsplash

Why is it important?

This study was designed to explore the effect of FC-99 on macrophage polarization in vitro and lipopolysaccharide- (LPS-) induced liver injury followed by the underlying mechanisms. For in vitro experiments, FC-99 inhibited M1-related macrophage factors and promoted M2-related markers induced by IL-4 in the mouse macrophage cell line. Moreover, FC-99-induced macrophages polarized to M2 phenotype which could be repressed by a PPAR-γ inhibitor but not STAT6 siRNA knockdown, indicating FC-99-induced M2 macrophage polarization through PPAR-γ rather than STAT6 signal. In LPS-induced septic mice, FC-99 pretreated mice displayed lower expression of M1 markers together with the increased M2 marker CD206 and improvement of liver injury.

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