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• W2022730022 abstract "Abstract Background and Aims: Activation of the pro‐inflammatory cytokine cascade, including tumor necrosis factor alpha (TNF‐α) is considered to play an important role in the pathophysiology and clinical outcome of severe liver injury. Kupffer cells, resident macrophages of the liver, have a transmembrane protein Toll‐like receptor 4 (TLR4), which recognizes endotoxin (lipopolysaccharide; LPS) or LPS‐CD14 complex and mediates macrophage activation and pro‐inflammatory cytokine release. d ‐Galactosamine (GalN), a hepatocyte‐specific inhibitor of RNA synthesis, is known to sensitize animals to the lethal effects of LPS and TNF‐α. In the present study we seek to address TLR4‐signaling in the development of GalN‐induced acute hepatic failure (AHF) and explore the expression of TLR4 mRNA as compared to TNF‐α mRNA and CD14 mRNA in the liver, spleen and lung of rats with GalN‐induced hepatitis. Methods: AHF was induced in male Wistar rats by the intraperitoneal injection of 1 g/kg bodyweight GalN. Expression levels of TNF‐α, TLR4 and CD14 mRNA in the whole liver, spleen and lung of rats were detected by reverse transcription–polymerase chain reaction analysis. Results: Expression level of TLR4 mRNA in the liver of rats with GalN‐induced AHF was increased parallel with that of TNF‐α and CD14 mRNA as compared to the control rats. However, expression levels of TNF‐α, TLR4 and CD14 mRNA in the whole spleen and lung were not different between rats with AHF and control. Conclusions: There may be a difference of stimulatory effects of endotoxin on the innate immunity between the liver and other organs of rats with GalN‐induced AHF." @default.
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• W2022730022 date "2008-07-31" @default.
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• W2022730022 title "Expression of Toll-like receptor 4 in various organs in rats with d-galactosamine-induced acute hepatic failure" @default.
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• W2022730022 doi "https://doi.org/10.1111/j.1440-1746.2007.05246.x" @default.
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