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. Author manuscript; available in PMC: 2011 Sep 1.
Published in final edited form as: Hepatology. 2010 Feb;51(2):621–632. doi: 10.1002/hep.23365

Figure 7. Absence of TLR9 combined with HMGB1 blockade increases hepatic resistance to I/R injury.

Figure 7

WT and TLR9−/− (A) CD45+ NPCs or (B) neutrophils were cultured in conditioned (Con) media from necrotic hepatocytes and αHMGB1. Certain wells containing αHMGB1 were pre-treated with DNAse I for 2 h. After 12 h or 24 h, supernatant cytokines were measured. (C) WT and TLR9−/− mice were injected with αHMGB1 or isotype control 1 h prior to I/R. Serum ALT was measured 12 h later. (D) The percentage of neutrophils in the ischemic livers of mice subjected to 12 h of I/R following treatment with αHMGB1 or isotype is shown. (E) WT mice were pre-treated with iCpG, αHMGB1 or both just prior to I/R. Serum ALT was measured 12 h later. Data represent means ± SEM and are representative of 3 (A, B) or 2 (C, D, E) independent experiments (4–6 mice/group). *p<0.05; **p<0.01.