Methylchlorogenic acid (MC) is one of the main components in the leaves of Eriobotrya japonica. We previously reported that MC is the most potent antioxidant among several components of Eriobotrya japonica, and its antioxidant activity is stronger than that of chlorogenic acid. Antioxidants are expected to inhibit redox-sensitive NFkappaB activation since NFkappaB is readily influenced by cellular oxidative state. Based on these findings, in vivo experiments with MC were conducted to determine its ability to downregulate the NFkappaB activation in mouse liver. Results clearly showed that MC is a potent suppressor of BHP-induced NFkappaB activation. We observed a significant reduction by MC on BHP-induced translocation of p65 subunit of NFkappaB. This may be due to formation of p50/p65 heterodimer, which is mainly inducible NFkappaB. MC slightly blocked the BHP-induced IkappaB alpha degradation. There is a possibility of IkappaB alpha resynthesis via activated NFkappaB during a 5 h waiting period following BHP injection. The present results suggest that MC may inhibit NFkappaB activation, exhibiting its ability to downregulate the NFkappaB-dependent gene expression. Thus, it can be expected that MC may have potential for therapeutic intervention on various NFkappaB-dependent pathological conditions such as inflammatory or possibly mutagenic processes.