Inhibition of NFκB by Methyl Chlorogenate from Eriobotrya japonica

Abstract

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 NFκB activation since NFκB 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 NFκB activation in mouse liver. Results clearly showed that MC is a potent suppressor of BHP-induced NFκB activation. We observed a significant reduction by MC on BHP-induced translocation of p65 subunit of NFκB. This may be due to formation of p50/p65 heterodimer, which is mainly inducible NFκB. MC slightly blocked the BHP-induced IκBα degradation. There is a possibility of IκBα resynthesis via activated NFκB during a 5 h waiting period following BHP injection. The present results suggest that MC may inhibit NFκB activation, exhibiting its ability to downregulate the NFκB-dependent gene expression. Thus, it can be expected that MC may have potential for therapeutic intervention on various NFκB-dependent pathological conditions such as inflammatory or possibly mutagenic processes.