Figure 7.

Reaction sequences illustrates the involvement of ageing and n‐butylidenephthalide in macrophage skewing‐ and myofibroblast‐mediated cardiac fibrosis after MI. Inflammatory M1 macrophages were dominant at the early stage of MI, however, anti‐inflammatory M2 phenotype was prevalent at a late stage. IL‐10 activity in M2 macrophages inhibits myofibroblast differentiation, which in turn reduces extracellular matrix production. n‐butylidenephthalide administration exhibits potent antifibrotic activity via increasing the activation of M2 macrophages and inhibiting myofibroblast differentiation. Inhibition of these signalling pathways by their respective inhibitors is indicated by the vertical lines