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. 2017 Jul 6;2(13):e92530. doi: 10.1172/jci.insight.92530

Figure 6. Increased glycolysis is responsible for iKIR-mediated animal mortality during sepsis.

Figure 6

Mice were treated with the competitive hexokinase inhibitor 2-deoxyglucose (2-DG; 0.5 g/kg, i.p.) daily for 4 days and 1 hour before cecal ligation and puncture (CLP). The animals were also treated with iKIR (inhibitor of the kinase inhibitory region), 24 hours and 1 hour before surgery. (A) Lactate levels in peritoneal exudate (n = 5–7 mice/group, 1-way ANOVA followed by Bonferroni correction). (B) Bacterial loads were determined in blood and peritoneal exudate 18 hours after CLP (n = 4–9 mice/group, 1-way ANOVA followed by Bonferroni correction). Levels of IL-1β (C) and TNF-α (D) were quantified in peritoneal exudate (n = 4–5 mice/group, 1-way ANOVA followed by Bonferroni correction). Scatter plot shows individual values, mean, and SEM. *P < 0.05, control-treated septic mice vs. naive; &P<0.05, iKIR vs. control-treated septic mice; %P<0.05, iKIR and 2-DG vs. iKIR-treated septic mice; #P<0.05, iKIR-septic mice vs. naive mice. PC, peritoneal cavity.