FIGURE 7.

Schematic diagram of the proposed mechanism underlying the protective effects of harmine on sepsis-induced cardiac dysfunction. Macrophages are activated by LPS and produce abundant inflammatory mediators (proinflammatory M1 phenotype). Harmine inhibits M1 macrophage polarization by suppressing the STAT1/3, MAPK, and NF-κB pathways and subsequently reduces the release of inflammatory mediators. Ultimately, it alleviates cardiac oxidative stress, inflammation and apoptosis in vitro and in vivo.