Fig. 3: The inhibition of S100A9, a downstream player of necroptosis signaling, alleviates acute hepatic injury, which is relevant to M2-like activation of macrophages. | Cell Death & Disease

Fig. 3: The inhibition of S100A9, a downstream player of necroptosis signaling, alleviates acute hepatic injury, which is relevant to M2-like activation of macrophages.

From: M2-like macrophages exert hepatoprotection in acute-on-chronic liver failure through inhibiting necroptosis-S100A9-necroinflammation axis

Fig. 3

a Serum S100A9 levels in control and acutely injured mice. (n = 6) b Comparison of S100A9 expression in the livers of acutely injured mice with or without necroptosis inhibitors. c Comparison of survival rates in acutely injured mice with or without S100A9 inhibitor. (n = 8–13) d The hepatic damage assessed by serum ALT levels in mice challenged by D-GalN/LPS with or without S100A9 inhibitors. (n = 5–8) e The hepatic damage assessed by histopathology with H&E staining in mice challenged by D-GalN/LPS with or without S100A9 inhibitors. f M1 macrophage activation marker iNOS and M2 macrophage activation marker CD206 expression in mice receiving D-GalN/LPS insult with or without S100A9 inhibitors. g M1 (iNOS) and M2 (Arg-1 and CD206) macrophage activation markers were assessed and compared by real-time PCR in mice receiving D-GalN/LPS insult with or without S100A9 inhibitors. *P < 0.05, ***P < 0.001. (n = 4–6).

Back to article page