Sepsis is a life-threatening disease. Inflammation is a major concomitant 
symptom of sepsis Chrysophanol, an anthraquinone derivative isolated from the 
rhizomes of rheumpalmatum, has been reported to have a protective effect against 
lipopolysaccharide(LPS)-induced inflammation. However, the underlying molecular 
mechanisms are not well understood. The aim of this study was to explore the 
effect and mechanism of chrysophanol on lipopolysaccharide (LPS)-induced 
anti-inflammatory effect of RAW264.7 cells and its involved potential mechanism. 
The mRNA and protein expression of tumor necrosis factor (TNF)-α, interleukin 
(IL)-1β and inducible nitric oxide synthase (iNOS), nuclear factor kappa B 
(NF-κB) and PPAR-γ were measured by qRT-PCR and western blotting, the production 
of TNF-α, IL-1β was evaluated by ELISA. Then, the phosphorylation of NF-κB p65 
was also detected by western blotting. And NF-κB p65 promoter activity was 
analyzed by the Dual-Luciferase reporter assay system as well. Meanwhile, PPAR-γ 
inhibitor GW9662 was performed to knockdown PPAR-γ expression in cells. Our data 
revealed that LPS induced the up-regulation of TNF-α, IL-1β, iNOS and NF-κB p65, 
the down-regulation of PPAR-γ were substantially suppressed by chrysophanol in 
RAW264.7 cells. Furthermore, our data also figured out that these effects of 
chrysophanol were largely abrogated by PPAR-γ inhibitor GW9662. Taken together, 
our results indicated that LPS-induced inflammation was potently compromised by 
chrysophanol very likely through the PPAR-γ-dependent inactivation of NF-κB in 
RAW264.7 cells.