Figure 1

Organ architecture serum inflammatory cytokine levels, and aminotransferase activities in septic mice treated with simvastatin or dLGG. (A) Chemical structure of simvastatin, a cholesterol-lowering drug and inhibitor of HMG CoA reductase, and 1,2-di-O-α-linolenoyl-3-O-β-galactopyranosyl-sn-glycerol (dLGG), a plant galactolipid isolated from Crassocephalum rabens. (B) Comparison of levels of proinflammatory cytokines, TNF-α and IL-6, in sera of mice treated with DMSO (vehicle control), 25 mg/kg dLGG (dLGG25 only), 5 mg/kg LPS (LPS) only, 10 mg/kg simvastatin (Simva10 + LPS) and low-dose (dLGG5 + LPS) and high-dose (dLGG25 + LPS) dLGG pretreatment and (LPS + dLGG25) posttreatment. Simvastatin and dLGG were administered 1 h prior to LPS in the pretreatment groups, and dLGG was administered 1 h after LPS in the posttreatment group (N = 4, P < 0.05, ANOVA, post hoc LSD; values with different letters are significantly different). (C) Levels of aminotransferases, aspartate aminotransferase (AST) and alanine aminotransferase (ALT), from the sera of mice from the vehicle control, and LPS and simvastatin and dLGG treatment groups (N = 4, P < 0.05, ANOVA, post hoc LSD; values with different letters are significantly different). (D) Pathological examination of organ morphology and architecture among the treatment groups by H&E staining. Integrity of portal veins in the liver, alveolar sacs in the lungs and renal glomeruli, as well as the presence of inflammatory cells in all the treatment groups were compared with the vehicle control treatment (scale bar = 100 µmol/L).