Lack of PPARÎ± exacerbates lipopolysaccharide-induced liver toxicity through STAT1 inflammatory signaling and increased oxidative/nitrosative stress

Article ID	Journal	Published Year	Pages	File Type
5860785	Toxicology Letters	2011	7 Pages	PDF

Abstract

âº Activation of STAT1 and NF-ÎºB inflammation signaling in LPS-exposed Ppara-null Mice. âº Elevation of pro-inflammatory cytokines and chemokines in LPS-exposed Ppara-null mice. âº Inhibition of anti-oxidant enzymes and mitochondrial complexes after LPS exposure. âº Increased lipid peroxidation and protein nitration in LPS-exposed Ppara-null mice. âº More severe LPS-induced acute liver damage in Ppara-null mice than WT mice.

Keywords

NF-κB ALT MCP-1 GPX PPARα CAT TNFR1 IFN-γ TLR 3-NT IL-6 LPS TNFα MDA 3-nitrotyrosine MPO H&E MAPK ROS acute liver damage Alanine aminotransferase STAT Oxidative/nitrosative stress interferon-γ interleukin-6 Terminal deoxynucleotidyl transferase dUTP nick end labeling tumor necrosis factor-α TUNEL SOD Superoxide dismutase Cytokines nuclear factor-κB lipopolysaccharide malondialdehyde signal transducers and activators of transcription myeloperoxidase wild-type Hematoxylin and Eosin Monocyte chemotactic protein-1 mitogen activated protein kinase Catalase glutathione peroxidase Reactive oxygen species Tumor necrosis factor receptor-1 Toll-like receptors