Figure 2
From: Kallistatin treatment attenuates lethality and organ injury in mouse models of established sepsis
Delayed kallistatin treatment reduces malondialdehyde (MDA), high mobility group box-1 (HMGB1) and toll-like receptor-4 (TLR4) expression, and increases suppressor of cytokine signaling-3 (SOCS3) expression in lung tissue of cecal ligation and puncture (CLP) mice. Levels of (A) MDA, (B) HMGB1 and (C) TLR4 were significantly reduced in kallistatin-treated mice (n = 3 to 4). (D) Kallistatin administration also significantly increased SOCS3 expression compared to the sham group (n = 3). Data are expressed as means ± SE. *P <0.05 versus sham group; # P <0.05 versus CLP control group.