Intestinal epithelial cells produce cytokines that play an important role in mucosal immune and inflammatory responses. Some natural agents can reduce inflammation inter alia by influencing on secretion of proinflammatory cytokines and chemokines. Phytic acid (IP6) is one of the bioactive compound that is present in cereals, legumes, oilseeds and nuts. It is, recognized to posses various significant health benefits including anticancer effects. Previous studies showed that it can also modulate immune functions of intestinal epithelium through regulation of the secretion of some interleukins, but mechanisms underlying that cellular response to IP6 have weakly been examined, as yet. One of the signal transduction pathways involved in a variety of inflammatory responses is p38 mitogen-activated protein kinase (MAPK) pathway.

The aim of this study was to examine the effect of IP6 on the p38 MAPK activity as well as to evaluate its influence on the expression of gene encoding p38 MAPK in unstimulated and IL-1β-stimulated Caco-2 cells. The effect of IP6 on IL-8 secretion by these cells and the interaction of IP6 with p38 MAPK signal transduction pathway were also studied. Cells were preincubated with p38 MAPK activator (anisomycin) and inhibitor (SB203580) followed by incubation with IP6. IL-8 levels were measured in the culture supernatants by ELISA.

In this study, the in vitro inhibitory effect of IP6 on recombinant p38 MAPK activity was demonstrated for the first time. Treatment of cells with IP6 for 3h resulted in a decreased p38 MAPK expression in both unstimulated and IL-1β-stimulated cells. Incubation of cells with anisomycin resulted in up-regulation of IL-8 secretion. Pretreatment of cells with anisomycin prior IP6 addition showed down-regulation of IL-8 secretion compared to the cells treated with anisomycin alone.

The study suggests that p38 MAPK could be one of the molecular targets for IP6 effects in the intestinal epithelial cells. These results also suggest that the effect of IP6 on IL-8 secretion by Caco-2 cells could be mediated by its inhibition of p38 MAPK activity.

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