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. 2013 Aug;59(2):318–326. doi: 10.1016/j.jhep.2013.04.014

Fig. 2.

Fig. 2

Cytokine response to sinusoidal injury. (A) Microarray suggested upregulation of the senescence associated chemokine CXCL1 in the liver of FOLFOX treated mice, which was confirmed by qRT-PCR (n = 8 animals per group). (B) Furthermore, CXCL1 was demonstrated to be elevated within the serum of mice with FOLFOX induced SOS (n = 9 animals per group). (C) qRT-PCR demonstrated upregulation of other senescence associated inflammatory mediators including CXCL2, MCP-1, and IL-6 (n = 8 animals per group). (D) IL-6 is more typically described as a pro-proliferative cytokine implicated in liver regeneration where it signals through activation of the transcription factor STAT3. Microarray and subsequent qRT-PCR demonstrated increased expression of this transcription factor in FOLFOX treated animals (n = 8 animals per group). Western blot demonstrated activation of this transcription factor by phosphorylation (E; representative blot of n = 6 per group), which immunohistochemistry revealed to be occurring predominantly in hepatocytes around portal tracts (F). Densitometry confirmed the increase in phosphorylated STAT3 seen on Western blot (F; n = 9 animals per group). ∗p <0.05; ∗∗p <0.01; ∗∗∗p <0.001. (This figure appears in colour on the web.)