AIM: To study the anti-inflammatory effects of aqueous extract from Dichroafebrifuga root (AEDF) for suppression in the process of lipopolysaccharide (LPS)-induced sepsis in the rat liver. METHODS: The inhibitory effect of AEDF on the alteration of inflammatory proteins was investigated by Western blot and immunohistochemical analysis. RESULTS: Western blot analysis showed that the level of nuclear factor (NF)-κBp65 was markedly up-regulated and (Ⅰ)κBα was down-regulated by LPS (8 mg/kg) challenge. However, AEDF 100 mg/kg inhibited induction of NF-κBp65 and degradation of Ⅰ-κBα in the liver of LPS-challenged rats. Immunohistochemical analysis showed that while the expression of the NF-κBp65, tumor necrosis factor (TNF)-α, and inducible nitric oxide synthase(iNOS) tended to increase, that of Ⅰ-κBα was decreased in the hepatocytes of rats challenged with LPS. A slight decline of NF-κBp65, TNF-α, and iNOS, but an increase of Ⅰ-κBα were observed in the hepatocytes of the rats pretreated with AEDF. CONCLUSION: AEDF may act as a therapeutic agent for inflammatory disease through a regulation of inflammation-related proteins. AIM: To study the anti-inflammatory effects of aqueous extract from Dichroafebrifuga root (AEDF) for suppression in the process of lipopolysaccharide (LPS)-induced sepsis in the rat liver. METHODS: The inhibitory effect of AEDF on the alteration of inflammatory proteins was Western blot analysis and immunohistochemical analysis. RESULTS: Western blot analysis showing that level of nuclear factor (NF)-κBp65 was markedly up-regulated and (I)κBα was down-regulated by LPS (8 mg/kg) challenge. , AEDF 100 mg/kg inhibited induction of NF-κBp65 and degradation of I-κBα in the liver of LPS-challenged rats. Immunohistochemical analysis showed that the expression of the NF-κBp65, tumor necrosis factor (TNF)-α, and Inducible nitric oxide synthase(iNOS) tended to increase, that of I-κBα was decreased in the hepatocytes of rats challenged with LPS. A slight decline of NF-κBp65, TNF-α, and iNOS, but an increase of I-κBα were Observed in the hepatocytes of The rats pretreated with AEDF. CONCLUSION: AEDF may act as an therapeutic agent for inflammatory disease through a regulation of inflammation-related proteins.