Quercetin is a common
antioxidant flavonoid found in vegetables, which is usually present in glycosylated forms, such as
quercitrin (3-rhamnosylquercetin). Previous in vitro experiments have shown that
quercetin exerts a bigger effect than
quercitrin in the down-regulation of the inflammatory response. However, such results have not been reproduced in in vivo experimental models of intestinal
inflammation, in which
quercetin did not show beneficial effects while its
glycosides,
quercitrin or
rutin, have demonstrated their effectiveness. In this study, we have reported that the in vivo effects of
quercitrin in the experimental model of rat
colitis induced by
dextran sulfate sodium can be mediated by the release of
quercetin generated after
glycoside's cleavage by the intestinal microbiota. This is supported by the fact that
quercetin, but not
quercitrin, is able to down-regulate the inflammatory response of bone marrow-derived macrophages in vitro. Moreover, we have demonstrated that
quercetin inhibits
cytokine and
inducible nitric oxide synthase expression through inhibition of the
NF-kappaB pathway without modification of
c-Jun N-terminal kinase activity (both in vitro and in vivo). As a conclusion, our report suggests that
quercitrin releases
quercetin in order to perform its anti-inflammatory effect which is mediated through the inhibition of the
NF-kappaB pathway.