$eta$-glycyrrhetinic acid (GA), the active principle of licorice (Glycyrrhiza glabra L.) has been reported to exhibit anti-inflammatory properties in different animal models. In this study, the effects of GA on the production of inflammatory mediators including tumor necrosis factor (TNF)-$alpha$, interleukin (IL)-6, nitric oxide (NO), and prostaglandin E (pGE)-2 were examined in RAW 264.7 cells in vitro. Furthermore, to elucidate a possible mechanism for the inhibitory effect of GA on the production of TNF-$alpha$, it was investigated whether the treatment of GA affects the I-${kappa}B{alpha}$ degradation and subsequent nuclear translocation of NF-${kappa}B$. Various inflammatory responses were induced in the culture system by treating with a lipopolysaccharide (LPS). GA showed anti-inflammatory activities in dose-dependant manner with $IC_{50}$ of $5.4{mu}M$ by inhibiting the production of TNF-$alpha$ in RAW 264.7 cells. In addition, the treatment of GA blocked both I-${kappa}B{alpha}$ degradation and the nuclear translocation of NF-${kappa}B$ from cytosol to nucleus. However, it did not affect the production of IL-6, NO, and PGE-2, implying the direct blocking of the production of TNF-$alpha$ resulting from both the I-${kappa}B{alpha}$ degradation and the nuclear translocation of NF-${kappa}B$. This finding might provide the underlying mechanism to explain the reported anti-inflammatory activities of GA in animal models.