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. 2016 Oct 18;12(12):2374–2385. doi: 10.1080/15548627.2016.1239678

Figure 2.

Figure 2.

HMGB1 is a late mediator of septic death in pink1−/− and park2−/− mice. (A) Time course of serum proinflammatory mediator levels in CLP-induced wild-type (WT), pink1−/−, and park2−/− mice with or without pramipexole (PRA; 1 mg/kg/i.p. at 2, 12, 24, and 48 h after CLP) treatment (n = 3 to 5 mice/group; *, P < 0.05 versus the group without PRA). (B) Survival after moderate CLP in pink1−/− and park2−/− mice with or without IgG (10 mg/kg/i.p. at +12, +24, and +48 h after CLP), HMGB1-neutralizing antibody (HMG1 Ab; 10 mg/kg/i.p. at +12, +24, and +48 h after CLP), and glycyrrhizin (Glz; 10 mg/kg/i.p. at +12, +24, and +48 h after CLP) (n = 10 mice/group; *, P < 0.05). (C and D) In parallel, tissue H&E staining (C) and serum enzyme activity (D) were assayed (n = 3 to 5 mice/group; *, P < 0.05 vs. IgG group). (E) Survival after moderate CLP in pink1−/− and park2−/− mice with or without IgG (10 mg/kg/i.p. at +12, +24, and +48 h after CLP), IL1B-neutralizing antibody (late: 10 mg/kg/i.p. at +12, +24, and +48 h after CLP; early: 10 mg/kg/i.p. at +2, +6, and +12 h after CLP) (n = 10 mice/group; *, P < 0.05).