Figure 4
From: Acid Sphingomyelinase Inhibition Prevents Development of Sepsis Sequelae in the Murine Liver

Preventative and therapeutic desipramine treatment abrogates sepsis-induced liver dysfunction in smpd1+/+ mice. Smpd1+/+ mice were treated either 7 days prior (preventative, p-smpd1+/+) or 6 hours (therapeutic, t-smpd1+/+) following sepsis induction with desipramine. (A) Serum SMPD1 activity (Fig. 4A; n = 4 smpd1+/+, n ≥ 6 p-smpd1+/+, t-smpd1+/+), (B) liver glutathion (GSH) levels (n = 4 smpd1+/+, n = 4 p-smpd1+/+, t-smpd1+/+), (C) γ-GT, (D) total serum bilirubin (n = 4 smpd1+/+, n ≥ 6 p-smpd1+/+, t-smpd1+/+) and (E) hepatic gene expression of Mrp2 (Fig. 4E; n = 4 smpd1+/+, n ≥ 5 p-smpd1+/+, t-smpd1+/+) are shown. Transcriptional expression is normalized to reference gene (Actb) and shown as log2 fold changes. Cut off values were set at ± 1, representing a variation of biological significance (dotted lines). #p < 0.05; ##p < 0.01 vs. corresponding smpd1+/+ control; *p < 0.05; * *p < 0.01 vs. baseline (MWU-test).