Abstract
Curcumin is a potential natural remedy for preventing
-associated gastric inflammation and cancer. Here, we analyzed the effect of a phospholipid formulation of curcumin on
growth, translocation and phosphorylation of the virulence factor CagA and host protein kinase Src
and in an
mouse model of
infection. Growth of
was inhibited dose-dependently by curcumin
.
was unable to metabolically reduce curcumin, whereas two enterobacteria,
and
, which efficiently reduced curcumin to the tetra- and hexahydro metabolites, evaded growth inhibition. Oxidative metabolism of curcumin was required for the growth inhibition of
and the translocation and phosphorylation of CagA and cSrc, since acetal- and diacetal-curcumin that do not undergo oxidative transformation were ineffective. Curcumin attenuated mRNA expression of the
virulence genes
and
in a dose-dependent manner and inhibited translocation and phosphorylation of CagA in gastric epithelial cells.
strains isolated from dietary curcumin-treated mice showed attenuated ability to induce cSrc phosphorylation and the mRNA expression of the gene encoding for IL-8, suggesting long-lasting effects of curcumin on the virulence of
. Our work provides mechanistic evidence that encourages testing of curcumin as a dietary approach to inhibit the virulence of CagA.