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Introduction The liver is the main metabolic organ of the human body, and it also metabolizes drugs and poisons. In most situations metabolism is accomplished without damage to the liver [...], Rosiglitazone, which is mainly used in the treatment of diabetes mellitus, is also involved in the regulation of inflammation. The peroxisome proliferator-activated receptor (PPAR)-γ receptor subtype appears to play a pivotal role in the regulation of inflammation. However, the exact mechanism for the protective effects of rosiglitazone against inflammation such as liver injury remains unclear. The aim of this study was to investigate the effects of rosiglitazone on inflammation in the liver of rats treated with D-GaIN/LPS. Male Sprague -Dawley rats were injected with D-GaIN/LPS with or without pre-administration of rosiglitazone (3, 10, or 30 mg/kg, intraperitoneal injection). Our data showed that rosiglitazone significantly inhibited D-GaIN/ LPS-induced hepatotoxicity in a dose-dependent manner, as indicated by both diagnostic indicators of liver damage (serum aminotransferase activities) and histopathological analysis. Western blot analysis showed that rosiglitazone significantly decreased protein expression levels of COX-2 and production of pro-inflammatory markers, including TNF-α and IL-6, in DGaIN/ LPS-treated rat liver. The results indicated that the inhibition of D-GaIN/LPS-induced inflammation by rosiglitazone can be attributed, at least partially, to its capacity to regulate the the immunoregulatory transcription factor nuclear factor kappa B (NF-κB) signaling pathway. Key words: rosiglitazone, liver injury, inflammation, D-GaIN/LPS, NF-κB, TNF-α, IL-6, COX-2. On rapporte que le rosiglitazone, principalement utilise dans le traitement du diabete sucre, est aussi implique dans la regulation de l'inflammation. Le recepteur PPAR-γ semble jouer un role pivot dans la regulation de l'inflammation. Cependant, le mecanisme exact de ses effets protecteurs envers l'inflammation comme le dommage hepatique demeure flou. Le but de la presente etude etait d'examiner les effets du rosiglitazone dans l'inflammation hepatique de rats traites au DGalN/LPS. Des rats males Sprague-Dawley ont recu une injection de D-GalN/LPS avec ou sans une administration prealable de rosiglitazone (3, 10 ou 30 mg/kg par voie intraperitoneale). Les donnees des auteurs ont montre que le rosiglitazone inhibait significativement l'hepatotoxicite induite par le D-GalN/LPS en fonction de sa concentration, comme l'indiquaient les indicateurs diagnostiques du dommage hepatique (activite des aminotransferases de serum) et l'analyse histopathologique. L'analyse par buvardage Western a montre que le rosiglitazone diminuait significativement les niveaux d'expression de COX-2 et la production de marqueurs pro-inflammatoires incluant le TNF-α et l'IL-6 dans le foie des rats traites au D-GalN/LPS. Les auteurs concluent que l'inhibition par le rosiglitazone de l'inflammation induite par le D-GalN/LPS est attribuable au moins en partie a sa capacite de reguler la voie de signalisation du facteur de transcription immuno-regulateur NF-κB. [Traduit par la Redaction] Mots-cles: rosiglitazone, dommage hepatique, inflammation, D-GalN/LPS, NF-κB, TNF-α, IL-6, COX-2.