“…The protective effect was associated with downregulation of the local expression of several potent proinflammatory cytokines, chemokine adhesion molecules, and neutrophil accumulation (2). PPAR␥ ligands have also inhibitory effects on generation of reactive oxygen species and lipid peroxidation in the liver (28,32). Consistent with these previous findings, in the present study we have demonstrated that ciglitazone reduced liver neutrophil infiltration in both age groups.…”
Zingarelli B, Chima R, O'Connor M, Piraino G, Denenberg A, Hake PW. Liver apoptosis is age dependent and is reduced by activation of peroxisome proliferator-activated receptor-␥ in hemorrhagic shock.
“…The protective effect was associated with downregulation of the local expression of several potent proinflammatory cytokines, chemokine adhesion molecules, and neutrophil accumulation (2). PPAR␥ ligands have also inhibitory effects on generation of reactive oxygen species and lipid peroxidation in the liver (28,32). Consistent with these previous findings, in the present study we have demonstrated that ciglitazone reduced liver neutrophil infiltration in both age groups.…”
Zingarelli B, Chima R, O'Connor M, Piraino G, Denenberg A, Hake PW. Liver apoptosis is age dependent and is reduced by activation of peroxisome proliferator-activated receptor-␥ in hemorrhagic shock.
“…Evidence from animal and human studies suggested that there is a correlation between the tissue MDA levels and the degree of burn complications, including shock and remote organ damage (32)(33)(34)(35). In the present study, burn-induced increase in the lung MDA levels were prevented by etanercept treatment, suggesting that antagonism of TNF- exerts a potent protective effect against lipid peroxidation.…”
“…Indeed, recent clinical studies indicated that PGC-1α agonists can alleviate post-burn insulin resistance (34,35) and prevent burn-induced damage in remote organs (36). That PGC-1ß is a highly inducible factor in most tissues and responds to common pathways of calcium and cAMP signaling strongly suggests that it may be possible to find drugs that induce PGC-1ß.…”
Abstract. Using a mouse model of burn trauma, we tested the hypothesis that severe burn trauma corresponding to 30% of total body surface area (TBSA) causes reduction in adenosine triphosphate (ATP) synthesis in distal skeletal muscle. We employed in vivo 31 P nuclear magnetic resonance (NMR) in intact mice to assess the rate of ATP synthesis, and characterized the concomitant gene expression patterns in skeletal muscle in burned (30% TBSA) versus control mice. Our NMR results showed a significantly reduced rate of ATP synthesis and were complemented by genomic results showing downregulation of the ATP synthase mitochondrial F 1 F 0 complex and PGC-1ß gene expression. Our findings suggest that inflammation and muscle atrophy in burns are due to a reduced ATP synthesis rate that may be regulated upstream by PGC-1ß. These findings implicate mitochondrial dysfunction in distal skeletal muscle following burn injury. That PGC-1ß is a highly inducible factor in most tissues and responds to common calcium and cyclic adenosine monophosphate (cAMP) signaling pathways strongly suggests that it may be possible to develop drugs that can induce PGC-1ß.
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