Berberine, an isoquinoline alkaloid, has a wide range of pharmacological effects, including anti-inflammation. It has been reported that berberine inhibits experimental colitis through inhibition of IL-8, and that inhibitory effect of berberine on inflammatory cytokine expression is mediated through peroxisome proliferator activated receptor (PPAR)-$gamma$. In this study, we examined the effects and action mechanism of berberine on the tumor necrosis factor (TNF)-$alpha$-induced monocyte adhesion to HT29 human colonic epithelial cells, which is commonly used as an in vitro model of inflammatory bowel disease (IBD). Berberine significantly inhibited the TNF-$alpha$-induced monocyte adhesion to HT29, which is similar to the effect of PDTC, a nuclear factor (NF)-$kappa$B inhibitor. However, ciglitazone and GW, the ligands of PPAR-$gamma$, did not suppress the TNF-$alpha$-induced monocyte adhesion to HT29 cells. In addition, TNF-$alpha$-induced chemokine expression and NF-$kappa$B transcriptional activity were significantly inhibited by berberine in a concentration-dependent manner. The results suggest that inhibitory effect of berberine on colitis is mediated through suppression of NF-$kappa$B and NF-$kappa$B-dependent chemokine expression.